StemCell Therapy

People with non-small cell lung cancer (NSCLC) may have an increased risk of severe illness from COVID-19. Guidelines advise people with NSCLC to follow the same protocols as others to protect themselves from the virus while maintaining their treatment schedule and getting the vaccine when their doctor advises.

If a person with NSCLC gets a SARS-CoV-2 infection, they may be at higher risk of severe complications. Additionally, the effects of the pandemic may mean that there are delays to cancer treatment and screening. Health experts advise those with lung cancer to reduce their risk of infection and potential complications by following prevention methods, such as hand washing, mask wearing, physical distancing, and receiving the vaccine when possible.

Evidence suggests that the COVID-19 vaccines are safe and effective for individuals with NSCLC and that these shots can help lower their health risks. This is also true for people currently receiving cancer treatments, such as immunotherapy and chemotherapy. However, these individuals may require close monitoring to identify potential side effects. It is also advisable to consult a doctor regarding a suitable vaccine schedule.

This article discusses the associations between NSCLC and COVID-19, as well as the potential risks and appropriate precautions.

According to the American Cancer Society, lung cancer is among the most common forms of cancer in the United States and the leading cause of cancer deaths. There are two main types of lung cancer: NSCLC and small cell lung cancer. Approximately 84% of lung cancer cases are NSCLC, which can be difficult to treat, as it is often less sensitive to the current treatment options than other cancers.

People with NSCLC can experience symptoms that include:

People with NSCLC are also vulnerable to infection. This is because the combination of the disease and its treatments, such as chemotherapy, leads to a weakened immune system. People with cancer have a higher risk of severe illness from COVID-19.

COVID-19 is a respiratory disease that also affects the airways and lungs. The condition can cause symptoms similar to those of NSCLC, such as a persistent cough, tiredness, and breathing difficulties. Other symptoms of COVID-19 may include:

According to the Centers for Disease Control and Prevention (CDC), people with some chronic medical conditions, including cancer, are more likely than other people to develop a severe illness from COVID-19. Severe illness from COVID-19 can result in:

The increased risk for people with NSCLC can be due to the cancer itself, the cancer treatment, or a combination of both. People with NSCLC are also more likely to have other risk factors for severe illness from COVID-19, such as smoking and older age.

A 2021 review highlights evidence indicating that people with lung cancers are more likely than people with other cancers to die from COVID-19. A history of smoking and the increased pressure that the pandemic has placed on respiratory services in hospitals could contribute toward this increased risk.

Lung cancer can also cause various other complications, including blood clots, heart problems, and neuropathy.

There are many possible treatment options for people with NSCLC. These include:

The best type of treatment will depend on several factors, including the spread of the cancer and the presence of other medical conditions. Treatment will typically involve a combination of approaches.

COVID-19 has caused major disruptions to cancer care worldwide. A 2021 study suggests that the increased pressure on services during the pandemic is the main cause of these disruptions.

The treatment for NSCLC commonly involves visiting a clinic or hospital. This approach may put people with NSCLC at a higher risk of developing COVID-19 and potentially severe complications. The treatments themselves also pose additional risks by affecting the immune system. For example, chemotherapy suppresses the immune system, which reduces the bodys natural defenses against infections and disease.

People with NSCLC should discuss the risks and benefits of different treatment approaches in the context of COVID-19. In some cases, a doctor may suggest delaying treatment to minimize the risk of complications. They may also suggest that people receive a COVID-19 vaccine before initiating cancer treatments, as this may improve the chances of an adequate immune response.

COVID-19 vaccinations are a safe and effective way of preventing severe disease and limiting the spread of the virus that causes it. The CDC states that COVID-19 vaccines have been subject to the most intense safety monitoring in U.S. history.

Health experts recommend that people with most underlying medical conditions, including cancer, get the vaccine. The risks of COVID-19 are far greater for people with cancer than the risk of rare side effects from the vaccine.

However, it is important for people with cancer to discuss with a doctor when is the right time to receive the vaccination. Some cancer treatments suppress the immune system and may reduce the effectiveness of the vaccine. People who have recently received cancer treatment may benefit from waiting until their immune system fully recovers before getting the vaccine.

People with NSCLC should take additional care to avoid getting COVID-19 due to the increased risk of severe disease. The National Cancer Institute recommends that people with cancer, or a history of cancer, keep safe and minimize the risk of getting a SARS-CoV-2 infection by:

NSCLC is a serious condition that requires treatment from a doctor. Early detection is vital to catching the cancer before it spreads and to improving treatment outcomes. Anyone who experiences any symptoms of NSCLC should contact a doctor immediately.

People living with NSCLC should also contact a doctor if they notice potential symptoms of COVID-19. A doctor can advise on testing and whether to visit a clinic in person or organize a home visit.

NSCLC is a common form of lung cancer that can be fatal. As both the condition itself and its treatments can affect the immune system and lungs, lung cancer puts a person at increased risk of potentially severe complications of COVID-19. It is advisable for people with NSCLC to follow guidelines on avoiding the virus, which include receiving the vaccine.

Evidence suggests that the vaccine is safe for people with NSCLC and that it can help provide adequate protection against SARS-CoV-2. A doctor can advise when to schedule a vaccine, which may be best before or after cancer treatments, so that it provides the optimal immune response.

Original post:
NSCLC and COVID-19: Risks and precautions - Medical News Today

I hate to be the voice of doom, but on top of the pandemic we are also facing an epidemic of allergic, asthmatic, and autoimmune disorders. You might be familiar with the first two, but when it comes to autoimmunity, most people only hear about it when they receive a diagnosis. It is certainly becoming one of the most common health concerns clients come to my clinic.

Autoimmune diseases include rheumatoid arthritis, lupus, multiple sclerosis, psoriasis, celiac disease, Hashimoto's thyroiditis, and the many other hard-to-classify syndromes of the 21st century. At their root they are connected by one central biochemical process, an immune imbalance. Your immune system gets confused and your own tissues get caught in a crossfire. Your body is fighting something - an infection, a toxin, an allergen even food, and somehow it redirects its hostile attack on your own tissues. This immune confusion results from what is referred to as molecular mimicry: when the invader's structure is very similar to the structure of our own tissue. Interestingly, autoimmune disorders occur almost exclusively in developed countries. People in poor nations without modern amenities like running water, flush toilets, washing machines, and manicured backyards don't get these diseases. If you grew up on a farm with lots of animals, you are also less likely to have any of these inflammatory disorders. Playing in the dirt and being exposed to bugs and infections trains your immune system to recognize what is foe and what is "you." Stress has a huge impact on your immunity, weakening your ability to fight infections and increasing your chances to develop allergies and autoimmunity.Autoimmune diseases when taken all together are a huge health burden. Unfortunately, many of the conventional treatments available can make you feel worse. When used selectively, these drugs can help people get their lives back. But they are not a long-term solution. Anti-inflammatory drugs and immune suppressants may lead to multiple side effects. They shouldn't be the end of treatment, but a bridge to cool off inflammation while the root cause of the disease is found and addressed.Naturopathy sees you as a whole, not as a machinery with separate parts. No matter what part of your body is under attack by your immune system, the solution is one and the very same: you need to find the root cause and balance your immune system using a functional medicine approach, a new way of thinking about the underlying causes and imbalances in chronic disease.You are also a unique individual a mixture of your genetic makeup, your history and your environment, therefore the only real solution is finding and addressing your specific cause, ridding your body and your environment of anything that may drive your condition, healing your damaged tissues by supplying your body with immune-balancing nutrients and powerful botanicals. The journey is long, it is not easy, but it leads to quality of life without side effects and halts the spread of autoimmunity to new tissues.

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Healthy Living: Autoimmunity the confused immune system - Limerick Leader

Data Presented at ASH Underscores the Potential of the Smart-Immune Platform That Can Generate ex-vivo T- cell progenitors and NK- Cells for the Treatment of Primary Immunodeficiencies, and Cancers

PARIS, Nov. 05, 2021 (GLOBE NEWSWIRE) -- Smart Immune SAS, a T-cell medicine company utilizing its proprietary ex-vivo biomimetic thymus in a dish technology to develop allogeneic T-cell progenitors Smart-101 (ProTcell) for rapid immune reconstitution, announced today the presentation of clinical data and preclinical research at the 63rd annual meeting of the American Society of Hematology (ASH), taking place December 11-14 in Atlanta, Georgia. Preliminary data in these abstracts became available on the ASH conference website 9:00 AM ET yesterday. Recently, Smart-Immune has also announced the commencement of its first US clinical trial using its T-cell progenitor product (Smart-101) for the treatment of patients with AML and ALL who receive allogeneic hematopoietic stem cell transplant (allo-HSCT).

For a young company like ours, the selection of abstracts at a prestigious hematology conference like ASH is a recognition of the potential of our platform technology to uniquely and selectively generate large numbers of T- and/or NK-progenitors with the purity and reproducibility necessary for clinical use, commented Karine Rossignol, the Chief Executive Officer and co-founder of Smart-Immune. These abstracts selected represent a decade of research by my co-founders Drs. Marina Cavazzana and Isabelle Andre to create a short and elegantly simple 7-day culture system to generate lymphoid progenitors allowing a fast (within 100 days instead of 1-2 years) a polyclonal reconstitution of a fully functional immune system able to fight cancers and infections, changing drastically the prognosis of patients. With widespread applicability across primary immunodeficiencies, and hematological cancers, and three clinical trials launched, Smart-Immune is the first company to bring allogenic human progenitor cells into clinical development.

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Abstracts accepted at ASH include:

1)

Rapid and Safe T Cell Immune Reconstitution By T Cell Progenitor Injection Following Haploidentical Transplantation for Severe Combined Immunodeficiency (SCID).

Presenter: Despina Moshous, Hospital Necker Enfants Malades

Session Name: 704. Cellular Immunotherapies: Clinical: Poster I

Session Date: Dec 11th, 2021

Session Time: 5:30 PM - 7:30 PM

Room: Georgia World Congress Center, Hall B5

Abstract Synopsis: Severe Combined Immunodeficiency (SCID), is a severe form of primary immunodeficiency, responsible for the death, within the first few months of life, if not treated with HSCT. In the absence of an HLA-identical HSC donor, an urgent haploidentical HSCT is proposed to newborns with Severe Combined Immunodeficiency (SCID). The authors describe how the Delta-4 ligand based, culture system, that is at the core of the Companys invention, can be used to generate the earliest CD7+ T-cell progenitors (Smart-101) from such a haploidentical donor. Patient outcomes for two SCID babies being treated in the ongoing Smart-Immune phase 1/2 trial in SCID, who receive Smart-101 after allogeneic HSCT is discussed. Available data indicate that when Smart-101 is used at the optimal window of time in the early weeks after birth, rapid immune reconstitution with CD3+, CD4+, CD8+ and CD19+ T-cells may result in freedom from infections and GvHD and can be lifesaving for such SCID babies. These preliminary results deserve further investigation, which will be performed as part of our ongoing clinical study.

2)

Ex Vivo Production Of Large Numbers Of Genetically Modified NK Cells From Cord Blood Or Mobilized Peripheral Blood CD34+ Cells Using Notch Ligand Delta-Like 4 Culture System

Presenter: Ranjita Devi Moirangthem, Smart-Immune SAS

Session Name: 703. Cellular Immunotherapies: Basic and Translational: Poster II

Session Date: Dec 12th, 2021

Session Time: 6:00 PM - 8:00 PM

Room: Georgia World Congress Center, Hall B5

Abstract Synopsis: In this research the authors extend the utility of the Companys proprietary Delta-4 ligand based, feeder free, culture platform from generating not just pure allogeneic T-cell CD7+ progenitors (Smart-101), but also being able to generate T-cell free, CD56+ NK-cells (Smart-103) when culture conditions are modified to be NK-conducive. Expansion of these NK-progenitors result in NK populations with normal surface markers, gene expression patterns and cytotoxicity seen in NK cells immunoselected from human beings. Allogeneic NK-therapy is at its infancy but provides many advantages over T-cell therapy in it being free from graft-versus-host disease and downstream cytokine storm in the recipient. Moreover, the Companys NK-cells are also easily gene modifiable such that the transgene is robustly expressed in the NK population, paving the way for possible future CAR- NK development expanding our technology to both lymphoid populations, i.e., T and NK cells.

At Smart-Immune, we are first and foremost focused on validating that our first cell-therapy product, which is our early progenitor T-cells (Smart-101) devoid of any form of genetic engineering, is of easy access and safe to patients in both the short-term and long-term, said Dr. Marina Cavazzana, co-founder and Chief Medical Officer of Smart-Immune. Smart-101 has to be safe and effective in what it is intended to do i.e., shorten the lymphoid immunodeficient period from 18 months to 3-6 months, benefiting infection, graft versus host (GvHD) and relapse rates, and possibly augmenting survival. Proving this in 2022-2023 will pave the way for our next phase of clinical programs starting early 2024 using CAR-ProTcell where our progenitor T-cells could bear efficient transgenes to fight cancers.

A description of all three US and European clinical trials using Smart-Immunes progenitor populations can be found on the Companys website: Smart-Immune.com

To learn more about the US clinical trial for Smart-101 in pediatric and adult leukemia, please refer to: ClinicalTrials.gov (Trial Identifier: NCT04959903)

About Smart Immune:Smart Immunes mission is to make T-cell therapy accessible and affordable to all patients and, through its groundbreaking ProTcell platform, has developed clinical stage T-cell progenitors designed to improve prognosis for patients affected by malignant blood diseases or rare primary immunodeficiencies. The company is utilizing its unique ex-vivo biomimetic thymus in a dish technology to culture specific T-cell progenitor subpopulations at clinical scale and use them for cell or gene therapy. The company was founded in 2017 by Dr Isabelle Andr, Karine Rossignol, and Dr Marina Cavazzana from Hpital Necker-Enfants Malades AP-HP, a pediatric hematologist and a pioneer in vector-based therapies and hematopoietic stem cell treatments.

About ProTcell:The Smart Immune ProTcell platform generates allogenic T-cell progenitors that provide fully functional polyclonal T-cells within 3 months following an allogeneic HSCT while also reducing GvHD, infections and relapses thereby reducing morbidity and mortality and improving the benefice risk ratio for allogeneic medicine. When infused, ProTcell progenitors migrate to the patients thymus where they expand, are selected, and then differentiate, resulting in fully functional T-cells, tolerant to the patients own immune system and reactive to viral, fungal, and malignant antigens. ProTcell has been accepted by the FDA as an Investigational New Drug (IND) for Acute Lymphocytic Leukemia (ALL) and Acute Myelocytic Leukemia (AML) and has also been granted fast track designation under its expedited program for serious conditions like SCID. In 2021, the FDA granted orphan drug designation for ProTcell as a treatment to enhance cell engraftment in patients receiving hematopoietic stem cell transplant (HSCT) including hematologic malignancies and all forms of primary immunodeficiencies. ProTcell is currently being studies in two clinical trials in Europe, with two in the U.S. expected to start in Q4 2021. To learn more, please visit http://www.smart-immune.com

Media/Investor Contact

Media Contact

Jason Wong

Clare Evans

Blueprint Life Science Group

Smart Immune

jwong@bplifescience.com

clare.evans.ext@smartimmune.com

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Smart Immune Announces Acceptance of Two Abstracts Covering Preclinical Research and Clinical Data at the American Society of Hematology - Yahoo...

A parasite commonly found in cats faeces might one day help treat cancer. My colleagues and I have discovered that the parasite that causes toxoplasmosis a condition that can be harmful to pregnant women and those with a suppressed immune system might be useful at destroying cancer tumours. At least, thats what our study in mice suggests.

For many years now, researchers have been looking at how they can use the bodys immune system to treat cancer known as immunotherapy. This is because, alongside protecting us from the harmful effects of bacteria and viruses, our immune system also rids the body of abnormal cells, such as cancer cells. But sometimes these cancerous cells and tumours can develop techniques for evading the bodys immune system, which means that the immune system wont kill them, and theyll be allowed to grow and replicate.

One type of immunotherapy is immune checkpoint blockade therapy. Our immune system contains a number of so-called immune checkpoints that prevent it from destroying healthy cells. But cancer cells can also avoid destruction by taking advantage of this on/off switch. The checkpoint can shut down immune cells called T cells and suppress the immune response. This is how some tumours are able to avoid being destroyed by the immune system.

Immune checkpoint blockade therapy works by blocking the checkpoint proteins from binding with their partner proteins and sending the off signal. This means that the cancer cells will become visible to the T cells, which can then go about destroying the tumour.

While immune checkpoint blockade therapy has shown promise in treating many types of cancer including lung cancer and melanoma this type of therapy, and many other immunotherapy treatments, dont work very well on so-called cold tumours. These difficult to treat tumours are surrounded by cells that suppress the bodys immune response, which means immune cells wont know how to attack it. Types of cancers where cold tumours are common include breast, ovary and prostate cancers.

But our latest research has discovered a method that could improve the treatment of these cold tumours and it involves using the parasite that causes toxoplasmosis, a relatively common condition that people catch from the faeces of infected cats or infected meat. While its typically harmless and often only causes mild flu-like symptoms, it can be serious in pregnant women and those who have a compromised immune system.

Toxoplasmosis is caused by the Toxoplasma gondii parasite. The reason we chose T. gondii is because it is very infectious and has been shown to infect many species of warm-blood animals including humans. The pathogen is also very tough, secreting proteins that prevent the bodys immune system from acting ultimately ensuring its own growth, replication and survival. We figured that all these attributes would allow T. gondii to trigger a strong immune response if administered directly into a tumour in the hope that would be enough for the immune system to kill the cancer.

Using the gene-editing technology Crispr, our team engineered a strain of Toxoplasma gondii that lacked the protein that causes disease. We then injected this mutant strain directly into melanoma tumours in mice. We later tested it on colon and lung cancer tumours as well.

We were able to show that injecting the live parasite directly into a cold tumour was able to trigger a strong immune response in mice. We were also able to show that even nearby tumours, which hadnt been injected, had an increased immune response.

While previous studies have shown that Toxoplasma gondii can be used to treat tumours in mice, our study took this finding one step further. We showed that when this engineered parasite was used alongside immune checkpoint blockade therapy, tumour growth was significantly suppressed. The eight mice given dual therapy in the early stages of melanoma saw their tumours shrink significantly, whereas treatment with only immune checkpoint blockade therapy failed to cause any regression in the injected tumours in mice.

We also showed that the dual treatment was far more effective at not only shrinking tumours but also improving the survival rate of mice when compared with using immune checkpoint blockade therapy alone. All eight mice who only received immune checkpoint blockade therapy died within 39 days while seven out of eight mice who received the dual treatment were still alive after 60 days. We also saw an increase in a number of different types of helpful immune cells which ultimately improved the response of melanoma tumours in particular to treatments.

Our research joins a body of evidence that parasites including the canine tapeworm Echinococcus granulosus can work against different types of cancer. Bacteria, viruses and bacteriophages (viruses that attack bacteria), are also being trialled as potential cancer treatments.

Its important to note that this study is only in mice, and it will take many years and many more studies before we know if this therapy works in humans. Nevertheless, its an exciting step in the right direction and adds to the growing evidence base that pathogens might be helpful tools in our fight against tough-to-treat cancers.

Read more:
A dangerous parasite could be used to treat cancer new research in mice - The Conversation UK

Facts about RSV and HMPV

When it comes to mosquito-borne diseases, malaria is among the worst. It claims thousands of lives annually worldwide and is widely considered an infection of the blood and liver. Also, the antibodies produced in response to the disease are well documented. However, scientists have reported the detection of an unexpected antibody produced against malaria in infected individuals: one that is made primarily in response to infections of the mucous membranes of different organs.

Through a multi-institutional study, researchers discovered the production of IgA (Immunoglobulin A) antibodiesthat are produced when the mucous membranes of organs such as the lungs are infectedin individuals infected with malaria. The study also found that the levels of IgA produced in children and adults in response to parasitic infection varied significantly.

"Not much had been done to study IgA antibodies in malaria infections, because people had not thought that they were important. Yet, because we were not looking for them, we may have missed a whole avenue of research that we can now explore," said Dr. Andrea Berry, corresponding author of the study, in a statement. The findings were published in the journal NPJ Vaccines.

Female anopheles albimanus mosquito (Representational Picture)Pixinio

Malaria is caused in human beings by five parasitic protozoa from the Plasmodiumfamily. They are transmitted through the bites of infected female Anopheles mosquitoes that serve as the primary vectors. Two of these protozoansPlasmodium falciparumand Plasmodium vivaxpose the biggest threats.

Several complications arise due to malaria. This includes damage to organs such as the kidneys and the liver, and can also result in the rupturing of the spleen. According to the World Malaria Reportreleased by the WHO in 2020, there were 229 million cases of malaria in 2019. The estimated number of deaths due to malaria was approximately 409,000 in 2019. Children below the age of five accounted for 67 percent (274,000) of all malaria deaths.

Different types of antibodies are produced by the immune system to help fight infections, and also to prevent reinfection. In older research, the authors had studied other antibody responses in patients with malaria. As expected, antibodies IgG (Immunoglobulin G), which is the most abundant antibody, and IgM (Immunoglobulin M), an antibody that appears during the initial phases of several infections, were detected.

Colorized scanning electron micrograph of red blood cell infected with malaria parasites, which are colorized in blue (Representational Picture)Flickr/ NIH Image Gallery

However, they also chanced upon an unexpected antibodyIgA (Immunoglobulin A). This was uncharacteristic as these antibodies are mostly produced in response to infections in the mucous membranes in areas such as the intestines, lungs, and vagina, among others. Therefore, the researchers chose to conduct a follow-up study to investigate additional samples for confirming their discovery and to scrutinize more groups of participants.

For the current study, the team examined antibody responsesboth IgG and IgAagainst P. falciparum in blood samples obtained from participants constituting three cohorts. The first group was composed of 32 individuals who had been infected through mosquito bites. Blood samples were collected on 1, 15, and 29 days post-infection.

The second group consisted of 22 volunteers who were challenged with the infection through direct intravenous (IV) introduction of P. falciparum. Blood samples were collected on 1, 29, and 57 days post-infection.

Red Blood Cells (Representational Picture)Wikimedia Commons

In addition to the two volunteer groups, the authors also collected samples from 47 childrenbetween the ages of one to sixliving in Mali, West Africa. These children were part of a malaria vaccine trial and their infections were naturally acquired during the course of the study.

Through their analysis, the researchers learnt that adult participants infected with malaria had high levels of IgA antibodies. The vaccine trial group consisting of Malian children exhibited a reduced prevalence of IgA antibodies. They also showed variability in the antigen specificity. However, ten children from the cohort had IgA antibody levels that were similar to those observed in adult participants.

The team also noted that patterns of IgG response were different between the three groups. Nevertheless, despite these variations, IgG antibodies were found to increase among all three cohorts. One question, however, remains to be answered: What leads to the development of IgA antibodies in malaria patients?

A mosquito biting a person (Representational Picture)Pxfuel

"We do not know what triggers the IgA antibodies to develop, but we think it happens early in a malaria infection. Some people think that the response might happen when the mosquito injects the parasiteinto the skin. Interestingly, some of our participants were not bitten by mosquitoes because their malaria infection was delivered intravenously, so there are probably additional triggers for IgA development," stated Dr. Berry.

It is not certain why the levels of IgA in children were not universally high. Dr. Berry averred that several reasons could be responsible for the differing levels of IgA. "Perhaps, children's immune systems respond differently to the parasite than adults do, or it is possible that IgA antibodies are only created during the first malaria infection," she posited.

Children (Representational Picture)Stocksnap.io

Deliberating on other potential reasons, Dr. Berry explained that the team was aware that the adult participants had received their first infection. However, it was not known whether the children in the vaccination trial had been infected previously.

While the timing of the infections and collection of samples among the adult volunteers was uniform, it was not the case among the child cohort. This was because their malaria infectionsoccurred coincidentally during the course of the study.

Dr. Berry added that tests can now be carried out to ascertain whether IgA antibodies prevent malaria parasites from entering red blood cells or the liver. She also said that the proteins which are targeted by IgA antibodies can be investigated and it can be gleaned whether they can be used in vaccines.

See more here:
Unexpected Antibody Type Discovered In Individuals With Malaria; New Insights Into Immune Response Against Disease [Study] - IBTimes India

Researchers at the University of Toronto have found that immune cells from the upper respiratory tracts of children, taken years before the pandemic began, react with the virus that causes COVID-19.

The findings hint at a possible reason why children with COVID-19 are often asymptomatic or have mild symptoms, while many adults experience severe disease and even death.

We isolated B cells from tonsil tissues collected from children over five years ago, and found that some are reactive to the SARS-CoV-2 spike protein, saidGoetz Ehrhardt, principal investigator on the study and an associate professor ofimmunologyat U of TsTemerty Faculty of Medicine.

We found that antibodies generated from these B cells have neutralizing potential against the virus in lab experiments, reducing the ability of the spike protein to bind to its target protein on the cell surface.

The study,published in theJournal of Immunology, is one of just a few to examine the role of the mucosal immune system in COVID-19. Other studies have looked at immune components in the bloodoften after infection has taken hold or during recovery.

Mucosal surfaces comprise one of the largest components of the immune systemand include the gut, urogenital tract and respiratory system all of which teem with microbiota including bacteria, viruses and fungi.

The researchers at first assumed the B cells reacted to SARS-CoV-2 because they had encountered similar coronaviruses in the past, perhaps through common colds and other infections.

But the antibodies did not react to those coronaviruses in further testing, although they did share genetic sequence characteristics linked to other triggers.

Taken together, Ehrhardt said, the results suggest cross-reactivity in the B-cell antibodies. The immune system makes these antibodies toward certain agents or pathogensand as a by-product the antibodies react to SARS-CoV-2, he said. It will be interesting to find out what causes that reaction.

A better understanding of the antibody reaction could shed light on the mystery of COVID-19 susceptibility in children and adultsand inform clinical and public health decisions as well as therapeutic approaches.

Whatever the cause of the reaction, it is likely due to a common element in the childhood environment sinceall samples the researchers tested had the SARS-CoV-2-reactive B cells many of which were observed also in the immune systems naive or newly generated B cells that had not encountered any pathogen.

One explanation is that some of these B cells react to triggers in the microbiome, saidYanling Liu, lead author on the paper and a senior research associate in Ehrhardts lab.

Or it could still be that antibodies are reacting to endemic coronavirusesand we just didnt see that, Liu said. We dont really know, but one implication of our work is that it suggests children should respond to vaccines very well since they have those naive B cells ready to recognize vaccine in their lymphoid tissue.

Several other researchers were key to the study, Liu and Ehrhardt said, includingJames Rini, a professor ofbiochemistryandmolecular geneticsat U of T who provided purified spike proteins from viral samples.

Amin Ziaused computational biology to scan large databases and predict which antibodies would react to the virus. Zia was a post-doctoral researcherin the lab ofAlan Moses, a professor in U of Ts departments ofcell and systems biology,ecology and evolutionary biologyandcomputer science in the Faculty of Arts & Science.

About half the antibodies we generated were based on computer-generated predictions, said Ehrhardt. That was first for us, and it wont be a last.

Researchers atthe Hospital for Sick Children, with whom Ehrhardts lab has collaborated for years, supplied the tonsil tissue samples.

Mucosae are no doubt a very important interface for the immune systems response to a great variety of pathogens, but availability of samples has been a major impediment, said Ehrhardt. Research in this area is gathering steam, and it will be interesting to see where that takes us.

The research was funded by the Canadian Institutes of Health Research.

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U of T research may help explain children's immune response to COVID-19 - News@UofT

"If it's not broken, don't fix it" is generally good advice for a lot of thingsyour favorite recipe, the gallery wall that took forever to put up, the workout routine your body has been lovingbut something it doesn't necessarily apply to? Your immune system.

While, no, you don't need to "fix" your immune system (nor could you), there are steps you can take to support it, even when you're feeling fantastic.

"Nothing is more critical for a healthy life than a well-functioning immune system," says clinical community pharmacist Kathy M. Campbell, PharmD. The goal, according to Dr. Campbell, is a Goldilocks approachyou want an immune system that's not too weak and not too strong.

"Nothing is more critical for a healthy life than a well-functioning immune system."

"A healthy, well-functioning immune system is an easy thing to take for granted," she says, but luckily, there are habits that can help support your immune systemsome of which you may already be doing. Eating nutrient-packed foods, prioritizing sleep, and getting some direct sunlight are all necessary for overall health, and they can also go a long way in supporting your immune system, Dr. Campbell says.

Assuming those habits are in check, turning to supplements for immune support can be a great next step. "Appropriately chosen, high-quality supplementation can be a very effective addition in supporting a healthy immune system," Dr. Campbell says.

Ready to start stocking up? First, talk to your healthcare provider. Next, turn to a trusted brand like Nature Made, which creates science-backed supplements for plenty of health needs, including immune support.

Okay, so yes, you want all of your supplements to be high-quality, but Dr. Campbell really emphasizes it for multivitamins. "It's important to provide a balance of all nutrients in an effort to minimize over-supplementation with a single nutrient," Dr. Campbell says. A high-quality multivitamin should do that balancing act for you.

Next up for supplements that support immune health? No surprise: good ole vitamin C. "Vitamin C is an essential nutrient, which cannot be synthesized by humans and therefore must be consumed by diet or supplementation," Dr. Campbell says. "Function is key in many biochemical processes within the immune system."

Vitamin D may already be high on your must-have list (hello, sunshine), but if you're supplementing with it, make sure to take it with vitamin K for the biggest impact, Dr. Campbell says. She also notes vitamin K can often be found in quality multis (pssstit's in Nature Made Women's Multivitamin Softgels). Vitamin D has multiple roles in the body, and can help support immune health, she says.

Optimal zinc levels help support a healthy immune system, Dr. Campbell says, but you'll also want to be careful not to overdue it. If you're supplementing with zinc, she recommends combining it with copper, which can often be found in multivitamins, likeyep, you guessed itNature Made Women's Multivitamin Softgels. Your immune system says thank you in advance.

Photo: Getty Images/shurkin_son

These statements have not been evaluated by the Food and Drug Administration. These products are not intended to diagnose, treat, cure or prevent any disease.

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Im a Pharmacist, and These Are My Top 4 Go-To Immune-Support Supplements - Well+Good

Sam Antonios| Special to The Capital-Journal

While viruses aren't new to humans, COVID-19 is novel to the human species, so no one has immunity against it. Like many other viruses, this novel coronavirus survives, replicates and transmits itself in and among its primary hosts: human beings.

Our human immune system fights off viral infections by developing special cells that secrete anti-virus molecules. But first, our bodies must learn how to build that immunity.

This coronavirus is a virus with which our bodies have had no previous experience. Some people's bodies can quickly create an immune response before the virus has the opportunity to overwhelm them, usually through domination of their respiratory system. Others aren't as fortunate and their immune system's response is too little, too late, causing them to fall victim to the disease.

For years, weve used vaccination to help our bodies ward off viral infections such as hepatitis, rubella, measles, chickenpox, influenza and rotavirus. The concept is simple: Introduce a non-active chunk or image of the virus so that our body becomes familiar with it and begins its immunity generation.

Because no actual virus has been introduced, that allows us to begin immunity stockpiling without the threat of disease. This model has helped humans for years and continues to do so with COVID-19.

After being vaccinated, when the body is exposed to the COVID-19 virus, it is more ready to fight it off, not even giving it a chance to overwhelm the body. COVID-19 can cause terrible medical problems and death to people. The vaccines available in the United States have been well-tested.

More than 388 million doses of the vaccines have been given in the U.S. and more than 6 billion doses worldwide. The goal is to develop enough collective immunity to stop this strain of coronavirus from spreading and mutating further the way viruses are designed to do.

Real-life evidence shows that the vaccines are working. Although people who have been vaccinated can still get a "breakthrough" infection and potentially transmit the virus, that infection tends to be milder because of their body's preparation work, thanks to the vaccines.

These infections occur far less frequently than those happening among unvaccinated people. We know this to be true because we are seeing this at our own hospitals and clinics.

This is why we continue to urge people to get vaccinated for COVID-19. While it might be tempting to try to ride this out, time is of the essence. The impact of this highly transmissible virus on the health and well being of our community is widely felt, as the surge commands significant resources, causing disruptions and delays for patients needing all types of care.

The story of our immune system fighting off invaders is long, this is simply another chapter. Using what we know works, we can beat this thing.

Sam Antonios, MD, is the chief clinical officer at Ascension Via Christi.

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'The story of our immune system fighting off invaders is long': COVID vaccination gives immune system a chance - The Topeka Capital-Journal

A microscopic image of a normal mouse small intestine. Cells stained red express normal amounts of cell-surface tags (MHC-II) needed by immune cells to find threats like infections or cancer. High-fat diets reduce the levels of MHC-II tags in intestinal cells, and so the immune system has a harder time recognizing intestinal tumors. Credit: Beyaz lab/CSHL, 2021

The immune system relies on cell surface tags to recognize cancer cells. CSHL researchers discovered mice who ate high-fat diets produced less of these tags on their intestinal cells, suppressing the ability of immune cells to identify and eliminate intestinal tumors. The high-fat diet also reduced the presence of certain bacteria in the mices gut, which normally helps maintain the production of these tags.

A high-fat diet increases the incidence of colorectal cancer. Cold Spring Harbor Laboratory Fellow Semir Beyaz and collaborators from Harvard Medical School and Massachusetts Institute of Technology have discovered that in mice, fat disrupts the relationship between intestinal cells and the immune cells that patrol them looking for emerging tumors. Reconfiguring the gut microbiome may be a way to heal the relationship.

The immune system patrols tissues looking for and eliminating threats. Certain immune cells look for tags that distinguish between normal and abnormal cells. One tag, called MHC-II, helps target cells for destruction. Cell-surface MHC-II activates the immune system to destroy that cell, whether it is just worn out or about to become cancerous. Beyaz and his colleagues found that when mice ate diets high in fat, MHC-II levels were suppressed in intestinal cells. Cells with reduced levels of these tags were not recognized as abnormal and thus could grow into tumors. Charlie Chung, a Stony Brook University graduate student-in-residence in Beyazs lab, says, If we alter the level of these immune recognition molecules in a positive way, then the tumor will more likely be recognized by the immune cell. We hope this can be coupled with the existing strategies, such as immunotherapy, to eradicate tumors.

Intestinal cells of a mouse that were fed a high-fat diet. The intestinal cells express less of the MHC-II tag than found in a gut from mice fed a normal diet. Credit: Beyaz lab/CSHL, 2021

The researchers found that a high-fat diet changed the mouses intestinal microbiome (the mixture of microbes in the gut). Several bacteria, including ones called Helicobacter, increase MHC-II, which may help immune cells locate abnormal cells. The team did a dirty roommate experiment where mice without these bacteria were housed with ones that had it. The clean mice became infected with the Helicobacter bacteria and produced more of the MHC-II tag.

The scientists findings suggest a new way to boost current immunotherapy treatments against cancer. Increasing the production of this MHC-II tag, either by diet, drugs, or changing the microbes in the body, can help the immune system recognize and eliminate cancer cells. Beyaz says:

This interaction between diet, microbes, and immune recognition has the potential to help us explain how lifestyle factors can contribute to tumor initiation, progression, or response to therapy.

Cancer cells use many tricks to avoid being recognized as abnormal by the immune system, but Beyaz hopes hes found several ways to outwit them.

Reference: Dietary suppression of MHC class II expression in intestinal epithelial cells enhances intestinal tumorigenesis by Semir Beyaz, Charlie Chung, Haiwei Mou, Khristian E. Bauer-Rowe, Michael E. Xifaras, Ilgin Ergin, Lenka Dohnalova, Moshe Biton, Karthik Shekhar, Onur Eskiocak, Katherine Papciak, Kadir Ozler, Mohammad Almeqdadi, Brian Yueh, Miriam Fein, Damodaran Annamalai, Eider Valle-Encinas, Aysegul Erdemir, Karoline Dogum, Vyom Shah, Aybuke Alici-Garipcan, Hannah V. Meyer, Deniz M.zata, Eran Elinav, Alper Kucukural, Pawan Kumar, Jeremy P. Mc Aleer, James G. Fox, Christoph A. Thaiss, Aviv Regev, Jatin Roper, Stuart H. Orkin and mer H. Yilmaz, 15 September 2021, Cell Stem Cell.DOI: 10.1016/j.stem.2021.08.007

Funding: National Cancer Institute, Oliver S. and Jennie R. Donaldson Charitable Trust, Mathers Foundation, STARR Cancer Consortium, Mark Foundation For Cancer Research, National Institutes of Health, Massachusetts Institute of Technology Stem Cell Initiative, Pew Foundation, Howard Hughes Medical Institute, American Association of Immunologists Career Reentry Fellowship

Continued here:
How High-Fat Diets Allow Cancer Cells To Go Unnoticed by the Immune System - SciTechDaily

Treatment for breast cancer is highly effective. Five-year survival rates for breast cancer have increased dramatically in recent decades, and much of that success can be credited to cancer researchers and campaigns designed to inform women about the importance of screenings.

Breast cancer is highly treatable, but treatment typically leads to some unwanted side effects. According to Johns Hopkins Medicine, women undergoing treatment for breast cancer may experience a host of side effects, including fatigue, pain, headaches, and dental issues. Cancer treatments, most notably chemotherapy, also can take a toll on womens immune systems.

Why does chemotherapy affect the immune system?

Cancer is caused by an uncontrolled division of abnormal cells in the body. According to Breastcancer.org, chemotherapy targets these abnormal cells, but also can affect fast-growing cells that are healthy and normal. So chemotherapy can damage cells throughout the body, including those in bone marrow. When bone marrow is damaged, its less capable of producing sufficient red blood cells, white blood cells and platelets. Breastcancer.org notes that the body is more vulnerable to infection when it does not have enough white blood cells.

Does chemotherapy always weaken the immune system?

The effects of chemotherapy on the immune system depend on various factors. According to Breastcancer.org, a patients age and overall health may influence the effects of chemotherapy on their immune systems. Young, healthy patients may be less vulnerable to infections from weakened immune systems than aging, less healthy patients. However, Susan G. Komen notes that the median age for breast cancer diagnosis in the United States is 63, so many patients are likely to be affected by the impact that treatment can have on their immune systems. The length of treatment and amount of medicines patients receive also can affect the impact of chemotherapy on patients immune systems. Breastcancer.org notes that being administered two or more chemotherapy medicines at once is more likely to affect the immune system than just one medication.

Chemotherapy is not the only treatment that can affect breast cancer patients immune systems. The Cancer Treatment Centers of America notes that surgery, radiation, CAR T-cell therapy, stem cell transplants, and even immunotherapy can affect the immune system. Surgery can overtax the immune system and compromise its ability to prevent infections and heal wounds caused by the procedure. Like chemotherapy, radiation therapy can damage healthy cells and lead to an increased risk of infection. And while immunotherapy is designed to boost the immune system by helping it recognize and attack cells more effectively, it also can lead to an overactive immune system that attacks healthy cells.

Cancer treatment is often highly effective. However, patients may need to work with their physicians to combat treatment side effects that can adversely affect their immune systems.

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How breast cancer treatments can affect the immune system - Defiance Crescent News

Booster shots now available at FAMU. Photo Courtesy: wctv.com

Florida A&M University is now offering two booster shots of the COVID-19 vaccine for those with compromised immune systems.

The Pfizer and Moderna third dosage are available to, but not limited to, individuals with acquired immunodeficiency syndrome (AIDS), lupus, heart conditions and people who are prescribed drugs that suppress their immune system.

Jamal Stokes, a Tallahassee native and lupus patient, has already received his booster shot for the Pfizer vaccine.

As soon as I got word that the booster shot was available on FAMUs campus, I went right up there, Stokes said. I didnt have to bring a doctors note or anythingvery grateful that the university is offering this.

The university is not requiring individuals with compromised immune systems to bring a doctors note to prove their conditions, preregister, or make appointments. They are only required to fill out a form upon arrival.

Tanya Tatum, the FAMU Student Health Services director, discussed the purpose of this third dosage for those who are eligible.

The additional dose brings their immune systems up to par with those who have healthy immunes and are fully vaccinated, Tatum explained.

Some students at the university are hopeful that the booster shot will eventually be offered to all individuals, no matter their immune status. Students are trying their best to remain optimistic about not only the future of the university, but the United States.

I think its really important that the campus is offering the third dosage and all other vaccines because hopefully that will encourage students to get it, Tyla Ewards, a fourth year facilities management student with long qt syndrome said. Its free and super convenient being that you can go get your booster shot in between classes with no hassle.

For now, scientists are recommending the booster shots to those with convincing evidence that the initial doses of the vaccine do not offer enough immune protection.

The Food and Drug Administration Advisory Committee has posed the question of whether to wait for a booster designed to fight against multiple variants to be offered to those with normal immune systems.

The most common side effects by clinical trial participants who have received the booster dose of the vaccine were pain, redness and swelling at the injection site. Other side effects include headache, fatigue, joint or muscle pain and chills.

Both Pfizer and Moderna Vaccines are available at FAMU on 659 Ardelia Court, located off Robert and Trudie Perkins Way. The site is open from 9 a.m. to 5 p.m. on Monday through Saturday.

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Booster shots now offered at FAMU The Famuan - Famuan

A new, sustainable immune health ingredient derived from carrot pomace is set to launch at the SupplySide West trade show in Las Vegas this October. Introduced by Dutch ingredients company NutriLeads (Wageningen, the Netherlands), BeniCaros is an ingredient suited for both dietary supplements and functional foods and beverages.

BeniCaros is a soluble fiber produced from upcycled carrot pomace, which is a byproduct of carrot juice production, making it a sustainable ingredient that is also label friendly.

NutriLeadss proprietary extraction process ensures the ingredient is rich in the immune-supporting polysaccharide rhamnogalacturonan-I (RG-I). The company says BeniCaros was shown in a clinical trial to help the immune system become more responsive to potential challenges as well as to stimulate beneficial gut microorganisms and their metabolites, at a daily dose of 0.3 grams. The firm says there is robust preclinical and clinical research showing the efficacy of BeniCaros.

In a press release, Ruud Albers, PhD, chief scientific officer for NutriLeads, said, I have been active in this field for more than 25 years and have never seen another ingredient with such distinctive data supporting its effectiveness. He added, There are many immune health ingredient options out there but very few that work like BeniCaros and even fewer that work with the same efficacy to support immune function.

Read more:
Immune health ingredient from carrots debuting at SupplySide West 2021 - Nutritional Outlook

Hospitals will begin contacting people over the age of 16, who have very weakened immune systems due to certain medical conditions, to offer them an additional Covid-19 vaccine.

Hospitals will identify the people who need an additional dose, the HSE said. You dont need to register or contact anyone.

People who need an additional dose will receive a text message with an appointment for their vaccine.

These additional doses will be given through a HSE vaccination centre near you, or your hospital if you are an inpatient. GPs may also vaccinate some people.

The HSE said this would happen from this week for those aged 16 and over.

As the vaccination programme for 12- to 15-year-olds started later, those aged 12 to 15 who have been identified for an additional dose will be offered an appointment at a later date.

This is to facilitate the two-month minimum interval from their last dose of Covid-19 vaccine.

Dr Colm Henry, Chief Clinical Officer of the HSE, said: It has been shown that people with weakened immune systems do not generate a full immune response to their first two doses of the Covid-19 vaccine.

This additional dose we are offering will mean they will get the maximum benefit from their primary vaccination course, giving them better protection against the serious effects of Covid-19.

It follows recommendations from the National Immunisation Advisory Committee (Niac) that people aged 12 years and older, who are immunocompromised at the time of vaccination due to disease or treatment, should receive one additional dose of a Covid-19 vaccine.

They will be offered a single dose of either Pfizer/BioNTech Covid-19 vaccine or Moderna vaccine. They need to continue to follow anti-Covid protection measures.

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Over-16s with weakened immune system to be offered third jab - Independent.ie

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A patient at The Ottawa Hospitals General campus has been diagnosed with legionellosis, forcing the hospital to turn off the water supply to a portion of the hospital in order to disinfect it.

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In a brief statement, the hospital said the water system at the General campus is undergoing hyperchlorination.

Ottawa Public Health said its infection prevention and control team was made aware of one case of legionellosis affecting a patient at the General campus and has worked closely with the hospital, locating the source and ensuring steps are taken to protect patients and staff.

There have been no further reports of legionellosis infection at The Ottawa Hospital, according to Ottawa Public Health. All cases must be reported to public health for follow up with the patient as well as investigation.

Ottawa Public Health performed environmental testing, with support from Public Health Ontario. The hospital continues to work with public health and has hired its own environmental consultants to lead the remediation.

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The illness is a form of pneumonia caused by exposure to Legionella, the common name for the bacterium L. pneumophila. It lives in water and may infect some people who inhale water droplets from a contaminated water supply, although most people will be unaffected.

For people with healthy immune systems the risk is low, but for those that have a suppressed immune system, there is a greater risk of infection, said the hospital.

The hospital said Tuesday it immediately turned off the water on the unit where the patient was, and the issue is being addressed.

During this time, water will be temporarily unavailable on certain units. We are working with care teams to ensure alternative water sources are available during this time, to minimize the impact on patient care.

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Rachel Muir, The Ottawa Hospital bargaining unit president with the Ontario Nurses Association, said the water has been shut off between the hospitals fourth and eight floors since the case of legionellosis was identified last Friday. She said the water isnt expected to be back on until later this week, possibly the weekend.

She said staff was notified last Friday that there was a case of legionellosis and the source was located in the water system in the unit.

Muir said drinking water and ice are being supplied to all the units affected and wipes and clean water are being provided for cleaning.

Patients will be freshened up but not showered until the system is back on.

Muir called it an inconvenience but said the hospital is working hard to minimize that and keep staff and patients informed.

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The hospital said it is working closely with public health and environmental experts to remediate the issue and to turn the water back on as soon as possible.

Legionnaires disease, named after a severe pneumonia outbreak at a convention centre in the U.S. in 1976, is the most common form of legionellosis. It can also cause less severe illness. According to the U.S. Centers for Disease Control and Prevention, healthy people usually get better after being sick with Legionnaires disease, but hospitalization is often required. About 15 out of 100 people who get it will die from the infection.

Many hospital patients have compromised immune systems because of illness, age or treatment. The General campus is home to The Ottawa Hospital Cancer Program where many patients are undergoing treatment that affects their immune systems ability to fight off infection.

Safety is our top priority, and we will continue to update patients and families to ensure they have all the information they need, said the hospital.

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Hospital disinfecting water system after patient at the General diagnosed with legionellosis - Ottawa Citizen

Lots of people these days are asking what they feel is a completely legitimate question, "Is it safe to get the COVID vaccine and get my flu shot?" The quick answer is: Yes. ABSOLUTELY...According to the Centers For Disease Control and Prevention.

WWLP/News 22 Springfield is reporting that, according to the CDC,its safe for other vaccines to be administered at the same time as the COVID-19 vaccine.

This new guidance is a definite change from previous CDC recommendations which said that other vaccinations should not be administered within a 2-week window before or after the COVID-19 vaccine.

With colder weather on the horizon, many people are starting to think about the flu shot in addition to COVID vaccinations. But there are also many who are wondering, after last year's very mild flu season, if getting a flu shot is even essential.

Health officials caution that substantial flu activity happening at the same time as COVID-19 activity could seriously overwhelm our health care systems.

The Centers For Disease Control and Prevention estimates that every year, anywhere between 12,000 to 61,000 people die due to the flu. Last year, however, the combination of social distancing and wearing masks prevented the majority of cases.

In summation, you can get your flu shot at the same time you get your COVID vaccination or vice versa. The CDC recommends getting the flu vaccine by the end of October and to get the COVID-19 vaccine as soon as you can.

For more information, check out WWLP's website here.

KEEP READING: See 25 natural ways to boost your immune system

Here are some tips for self-care during the pandemic:

KEEP READING: 15 Natural Ways to Improve Your Sleep

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Health Officials Addressing Concerns Over Flu Shot, COVID Shot - Live 95.9

A recent study has found that despite effective antiretroviral therapy, low CD4/CD8 ratios and high CD8 counts are associated with a higher risk of Kaposis sarcoma and non-Hodgkin lymphoma, respectively. This increased risk is particularly present in people living with HIV who have CD4 cell counts above 500.

As expected, virological failure was a strong risk factor for both cancers. Findings are published in Clinical Infectious Diseases.

Kaposis sarcoma is a cancer that forms in the lining of blood and lymph vessels. The tumours can appear as painless purplish spots on the legs, feet or face, in the genital area, mouth or lymph nodes, and may also develop at a later stage in the digestive tract or lungs. The underlying cause of Kaposis sarcoma is infection with a virus called human herpes virus-8 (HHV-8). This virus causes no symptoms in healthy people. However, in people with a damaged immune system CD4 loss, but also an imbalance between CD4 and CD8 cell counts which allows it to multiply, HHV-8 has the potential to trigger Kaposis sarcoma.

Non-Hodgkin lymphoma is a type of cancer that begins in the lymphatic system, which is part of the bodys germ-fighting immune system. In non-Hodgkin lymphoma, lymphocytes grow abnormally and can form tumours throughout the body. Signs and symptoms may include swollen lymph nodes, abdominal pain, persistent fatigue, night sweats, fever, chest pain, coughing or trouble breathing. Non-Hodgkin lymphoma can be induced by the Epstein-Barr virus (EBV), herpes virus-8 (HHV-8) or human T-cell leukaemia/lymphoma virus-1 (HTLV-1) when the damaged immune system cannot regulate them adequately.

A molecule on the surface of some white blood cells. Some of these cells can kill other cells that are infected with foreign organisms.

Lesions on the skin and/or internal organs caused by abnormal growth of blood vessels. In people living with HIV, Kaposis sarcoma is an AIDS-defining cancer.

A type of cancer that starts in the tissues of the lymphatic system, including the lymph nodes, spleen, and bone marrow. In people who have HIV, certain lymphomas, such as Burkitt lymphoma, are AIDS-defining conditions.

A group of lymphomas (cancers of the lymphatic system). The many types of non-Hodgkin lymphoma (NHL) are classified according to how fast the cancer spreads. Although the symptoms of NHLs vary, they often include swollen lymph nodes, fever, and weight loss. Certain types of NHLs, such as Burkitt lymphoma and immunoblastic lymphoma, are AIDS-defining cancers in people with HIV.

A type of lymphoma. Lymphoma is a cancer of a part of the immune system called the lymph system. The first sign of Hodgkin disease is often an enlarged lymph node. The disease can spread to nearby lymph nodes, the lungs, liver, or bone marrow. The exact cause is unknown. See also non-Hodgkin lymphoma.

Despite the widespread use of effective antiretroviral therapy and the resulting long-term viral suppression and CD4 restoration, a higher incidence of Kaposis sarcoma and non-Hodgkin lymphoma persists in people living with HIV, compared to the general population. These events seem to be driven by immune activation and inflammation that even viral suppression may not control.

CD8 cells are part of the immune system: also known as T killer cells, they recognise and destroy cells infected with viruses or bacteria. CD8 cell counts increase in response to acute infections. However, they can remain high in chronic infections such as HIV and respond to treatment more slowly than CD4 cell counts.

The CD4/CD8 ratio is considered a reliable marker of immune activation during successful antiretroviral therapy. Its normal value ranges between 1 and 4. When it is lower than 1 in people with HIV receiving antiretroviral therapy, it correlates with the risk of AIDS-related mortality and non-AIDS defining events, especially cancers.

However, the impact of the CD4/CD8 ratio on the risk of AIDS-defining cancers, such as Kaposis sarcoma and non-Hodgkin lymphoma, had never been studied before.

Dr Fabienne Caby and colleagues from COHERE (Collaboration of Observational HIV Epidemiological Research Europe, composed of several major cohorts) used data from over 50,000 people living with HIV who were receiving effective antiretroviral therapy to assess the impact of the CD4/CD8 ratio on Kaposis sarcoma or non-Hodgkin lymphoma risks in this population. This analysis focused specifically on whether or not this biomarker provided additional information to the CD4 count, which is the usual immunological predictor for both cancers.

As starting antiretroviral therapy with a high CD4 count is more and more common, the investigators conducted a secondary analysis that focused only on people with CD4 cell counts above 500 after they achieved virological control.

To be included in the study, individuals had to be at least sixteen years old, to have started antiretroviral therapy in the 2000-2014 period and to have achieved virological control defined as viral load below 500 copies within nine months after starting their treatment. At least one CD4/CD8 measurement, done in the six months following virological control, was needed.

For both analyses, the baseline was considered as the time of the very first CD4/CD8 ratio measurement within six months after virological control. Individuals with a diagnosis of Kaposis sarcoma or non-Hodgkin lymphoma at baseline or before could not be included in the study.

To better understand the impact of immune factors on the risk of the two cancers, three statistical models were tested, respectively adjusted for the CD4/CD8 ratio; both the CD4 and the CD8 cell counts; and for both the CD4/CD8 ratio and the CD4 cell count. All models were also adjusted for virological failure, demographics and year.

Overall, 57,708 people living with HIV from twenty cohorts in twelve Western European countries were eligible for the study. Men who have sex with men accounted for 49% of these participants, and women for 25%. Most participants were of European origin (69%), whereas 15% were of sub-Saharan origin (5770 women and 2691 men).

At baseline, the median age was 38 years (interquartile range 32-45) and the median CD4 and CD8 counts were 414 (IQR = 296-552) and 936 (IQR = 670-1304), respectively. The median CD4/CD8 ratio was low at 0.43 (IQR = 0.28-0.65) and reached 1 in only 8% of participants. Also, a very low CD4/CD8 ratio (<0.5) was found in 59% of participants.

Finding these low CD4/CD8 ratios in people with a suppressed viral load is not uncommon. As explained above, CD8 cells take time to respond to HIV treatment, except when treatment is started during acute HIV infection.

Participants were followed up for a median of 59 (IQR = 30-96) months from baseline, accounting for 307,700 persons-years. Two years after baseline, the CD4/CD8 ratio was restored to 1 in only 28% of participants (46% of those with a baseline CD4 count over 500).

In the primary analysis, Caby and colleagues found that during follow-up, Kaposis sarcoma and non-Hodgkin lymphoma had been diagnosed in 221 and 187 cases, respectively. This corresponded to incidence rates of 72/100,000 persons-years for the former and to 61/100,000 persons-years (95% CI; 46-76) for the latter. Most cases of Kaposis sarcoma were diagnosed between 2 to 37 months after baseline, whereas non-Hodgkin lymphoma was diagnosed between 7 to 42 months.

Of note, 15% (33/221) of Kaposis sarcoma cases and 12% (23/187) of non-Hodgkin lymphoma cases occurred in a context of virological failure.

The secondary analysis showed that among the 19,133 participants with CD4 cell counts above 500 at baseline, 65 were diagnosed with Kaposis sarcoma and 50 with non-Hodgkin lymphoma. However, this time, occurrence of the two cancers in a context of virological failure amounted to 14/65 cases (21%) of Kaposis sarcoma and 11/50 cases (22%) of non-Hodgkin lymphoma, despite the patients high CD4 cell counts.

What were the risk factors associated with Kaposis sarcoma? In all three models described above, virological failure was the strongest, with a nearly 3-fold higher risk (hazard ratio 2.77 in the third model).

When the CD4/CD8 ratio was looked at as the only immune factor, the lower it was, the higher the risk. When CD4 and CD8 counts were looked at separately, their independent associations with the risk of Kaposis sarcoma were confirmed.

In the third model which was found to be the most accurate CD4 counts and CD4/CD8 ratios were found to be independently associated with Kaposis sarcoma. The better the CD4 restoration was, the lower the risk: hazard ratio from 1.57 with 350 CD4 cells, to 0.71 with 650 CD4 cells, when compared to 500 CD4 cells. Furthermore, the association between the CD4/CD8 ratio and the risk of Kaposis sarcoma was gradual: hazard ratio from 1.18 in participants with a CD4/CD8 ratio of 0.8, to 2.02 in those with a CD4/CD8 ratio of 0.3, when compared to a normal CD4/CD8 ratio of 1.

The investigators highlight that in participants with CD4 cell counts above 500, the association between the CD4/CD8 ratio and the Kaposis sarcoma risk was stronger than that seen in the entire study population. They also found that being a man who has sex with men and being older were associated with a higher Kaposis sarcoma risk.

As observed with Kaposis sarcoma, virological failure was a strong factor for non-Hodgkin lymphoma risk, increasing it two-fold. Contrary to what was seen with Kaposis sarcoma, the CD4/CD8 ratio was not as predictive as the CD4 count for non-Hodgkin lymphoma.

However, the model adjusted for the CD4 and the CD8 counts showed that the risk for non-Hodgkin lymphoma strongly increased when the CD8 count was very high: hazard ratio from 1.61 for 2000 CD8 cells, to 3.14 for 3000 CD8 cells, compared to 1000 CD8 cells. This association was even stronger among participants with CD4 cell counts above 500 at baseline.

The investigators identified being older and male sex as other independent factors associated with a higher non-Hodgkin lymphoma risk.

These results confirm that HIV-related diseases still occur in people living with HIV despite a suppressed viral load and a relative immune response restoration. HIV-related inflammation is reflected in persistently high CD8 cell counts and leads to unbalanced CD4/CD8 ratios, raising the risk of AIDS and non-AIDS-related diseases.

Caby and colleagues say that CD4/CD8 ratios and high CD8 counts may be biomarkers of particular interest to people living with HIV who have high CD4 counts. For those with persisting low CD4/CD8 ratios despite efficient antiretroviral therapy, closer monitoring could be beneficial.

However, they add, further studies are needed to clarify the impact of the CD4/CD8 ratio on the risk of other HIV-related diseases, to know which specific preventative measures could be implemented.

See the article here:
Increased risk of Kaposi's sarcoma with low CD4/CD8 ratios and of non-Hodgkin lymphoma with high CD8 counts despite effective HIV treatment - aidsmap

RESEARCHERS have discovered a "cold environment" in a form of cancer which hides it from the immune system.

The findings mean immunotherapy- an emerging and advanced treatment which triggers the bodys own immune system to attack cancer cells - is unlikely to be effective in treating neuroendocrine tumours, a form of cancer which goes undetected by the immune system.

As a result, attention can now turn to understanding why this type of cancer is not recognised and finding ways to trigger an immune response to enable further treatments to be developed.

In this study, Dr Lulu Tanno, NETs research fellow at the University of Southampton, and her team studied samples of the tumours of 192 patients with pancreatic and small intestinal NETs at University Hospital Southampton.

The results, presented at the European Neuroendocrine Tumours Society, showed neither of these tumours contained any immune cells, known as tumour infiltrating lymphocytes (TILs), compared to hundreds found in the most common form of lung cancer.

Prior to this study very little was known about the quality and significance of the immune (anti-tumour) response in NETs but it is vital we know more with the emergence of immunotherapy as a potential treatment option, explained Dr Tanno.

What we have established is that there is no evidence of immune cells in pancreatic and small intestinal NETs, making it an immunologically cold environment and, therefore, unlikely to respond to current immunotherapy.

NETs are rare types of cancer which are usually found in the pancreas, bowel or lungs but can also develop in other parts of the body.

They arise from cells found throughout the body which form a link between the nervous system and the endocrine system, a collection of glands which produce hormones.

Around 4,000 new cases are diagnosed every year in the UK, though it is thought that a larger number of people are affected but remain undiagnosed as the cancers are slow growing.

If detected early they can often be cured with surgery but, at present, most are diagnosed at a later stage when they have already spread to other parts of the body.

Dr Tannos research programme was founded by the Robert White Legacy Fund and is part-funded by PLANETS Charity, which helps patients with pancreatic, liver, colorectal, abdominal and neuroendocrine cancer by funding patient support groups, innovative treatments and research.

She said NET patients curiosity and enthusiasm for knowing more about their condition was one of the major driving forces behind this research project.

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Researchers discover 'cold environment cancer' which hides from the immune system - Daily Echo

As the subject of the 2018 Nobel Prize in Medicine, tumor immunotherapy has proven to be an exciting cancer treatment strategy. Most immunotherapies to date have focused on T cell function; however, more natural killer (NK) cell-based therapies that involve monoclonal antibodies (mAbs) that target tumor antigens are emerging. mAbs have shown clinical success for the treatment of both hematological cancers and previously difficult to treat solid tumors. One fundamental mechanism through which mAbs can kill tumor cells is antibody-dependent cellular cytotoxicity (ADCC). ADCC refers to when mAbs elicit an immune response through the activation of NK cells and is triggered by the bi-specific binding of an antibody to both a NK cell activation receptor (CD16) and a target cancer cell protein antigen. This binding results in the release of cyto-toxic molecules that lead to targeted cancer cell death. While promising, mAbs are potentially immunogenic, can degrade in vivo and experience difficulties trafficking to the site of solid tumors. Furthermore, large doses of the mAb need to be administered intravenously. This increases manufacturing costs, resulting in higher drug prices and limiting general patient accessibility. An approach to utilize tumor immunotherapeutic antibodies directly in vivo using small immune recruiting molecules coined as covalent immune recruiters (CIRs) was developed. CIRs selectively link to naturally abundant serum antibodies and redirect them to the sur-face of tumor cells. The resultant display of tumor coated antibodies activates stimulatory receptors on innate immune cells, such as CD16 on NK cells, and triggers an antitumor immune response. The efficacy of these CIRs as modulators of protein proximity can be characterized by the Octet Bio-Layer Interferometry (BLI) platform. Octet systems are capable of real-time, high-throughput analysis of small molecule and biomolecule binding kinetics under equilibrium conditions. Due to its flexibility and compatibility for alternative assay format arrangements, it is a powerful tool for characterizing the CIR dependent binding equilibrium (e.g., tumor antigen:CIR:Ab) in addition to its use in determining CIR-antibody covalent recruitment kinetics. The label-free and highly sensitive nature of the Octet BLI technology also enables analysis under dilute conditions, conserving expensive biologic reagents and attenuating aggregation phenomena intrinsic to isothermal titration calorimetry (ITC) and fluorescence polarization (FP) assays. Octet systems also present a unique method to simultaneously characterize multiple protein binding and covalent labeling processes and discern reversible binding from a covalent reaction. Octet system can be employed to efficiently characterize CIR binding affinities against both a prostate tumor antigen and human serum antibodies, as well as measure the selective covalent recruitment of these antibodies to the tumor antigen. These assays can accelerate the advancement of lead compounds to in vivo validation studies, and have additional utility in characterizing emerging classes of covalent inhibitor drugs.

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Synthetic Immune Recruitment - A New Way to Fight Tumors - Technology Networks

It's "an arithmetic inevitability" that some people vaccinated against the coronavirus will contract so-called "breakthrough" infectionsbut a vaccinated person's immune system responds to the virus in distinctive ways that dramatically reduce the risk of serious disease, Katherine J. Wu writes for The Atlantic.

Your top resources on the Covid-19 vaccines

According to the Washington Post, it's difficult to track the absolute rate of breakthrough infections, both because many such infections are asymptomatic and because surveillance testing has declined in areas where vaccines are readily available.

It's clear, however, that breakthrough infections are uncommon and very rarely cause serious disease. According to CDC director Rochelle Walensky, 97% of all Covid-19 hospitalizations and 99.5% of all Covid-19 deaths are currently among the unvaccinated.

So why are breakthrough infections so much milder? It's because a vaccinated person's immune response looks very different than an unvaccinated person's, Wu writes.

When an unvaccinated person is exposed to the coronavirus, Wu writes, their only protection comes from the body's innate defenders, which are "short-lived and woefully imprecise."

"They'll sink their teeth into anything they don't recognize, and are easily duped by stealthier invaders," Wu writes, making them "a pretty flimsy first line of defense."

If left to its own devices, an unvaccinated person's so-called "adaptive" immune system will eventually develop a more powerful, customized response to the coronavirusbut it can take weeks to do so.

By then, Wu writes, "the virus may have run roughshod over everything it can." It may be too late for the immune system to prevent serious long-term damage or even death.

By contrast, a vaccinated person's immune system has already been trained to mount that more powerful, adaptive response. Vaccine shots "act as confidential informants, who pass around intel on the pathogen" before an infection occurs, Wu writes.

In particular, vaccination prepares the body's adaptive B cells to more quickly produce antibodies when they encounter the coronavirus, and T cells can more quickly target and kill off infected cells. This enables a vaccinated person to mount a powerful immune response much more quickly.

"In the best-case scenario, the virus might even be instantly sniped at by immune cells and antibodies," Wu writes. But even if the virus overwhelms the body's initial defenses, the vaccine has prepared the body to mount a fuller response.

"A breakthrough, despite what it might seem, does not cause our defenses to crumble or even break," Wu writes. "[I]t does not erase the protection that's already been built."

Rather, according to Deepta Bhattacharya, an immunologist at the University of Arizona, the virus must overcome "backup layer after backup layer" of defenses. So even if a virus continues to spread through a person's body, "[e]ach stage it has to get past takes a bigger chunk" out of it, Bhattacharya said.

That's why people who have been vaccinated tend to experience fewer and milder symptoms and recover more quickly, Wu writes.

"People tend to think of this as yes or noif I got vaccinated, I should not get any symptoms; I should be completely protected," Laura Su, an immunologist at the University of Pennsylvania, said. "But there's way more nuance than that."

"The vaccines were developed to keep us out of those terrible institutions we call hospitals," William Schaffner, an infectious disease expert at Vanderbilt University, said. "We have to keep coming back to that." (Gale, Washington Post, 7/25; AP/Modern Healthcare, 7/21; Cohen, Forbes, 7/22; Wu, The Atlantic, 7/26)

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Your immune system responds very differently to a 'breakthrough' Covid-19 infection - The Daily Briefing

Get ready to have a cold. Thats the message from doctors, immunologists, virologists and architects as England emerges from lockdown.

An amalgamation of 16 months cooped up inside, a culture of showing up to work despite sickness, and woefully outdated building infrastructure in the UK is set to become a pressure cooker for viruses. The country at large is about to experience the rush of a kind of post-lockdown Freshers Flu.

Never before in modern human history have we had global distancing, social distancing, mask wearing, quarantining and isolating, says Gregory Poland, head of the Vaccine Research Group at the Mayo Clinic in the US. Its going to be an interesting experiment of nature to see what happens when you stop the circulation of those viruses for a season.

Like Covid, colds are spread through inhaling droplets from the air, and also by touch. Under normal circumstances, the average adult has between two and four colds a year, while children have between six and eight. These move easily between people and can be contagious for up to two weeks after symptoms appear.

Pre-pandemic, our bodies were often exposed to viral respiratory pathogens. Sometimes these made us sick, and other times they boosted our immune responses. But lockdowns, increased hand washing, and masks may have dulled this risk and left a hole in our natural defences.

The hygiene hypothesis posits that early exposure to a variety of germs builds better immunity for life. As such, evidence suggests children who are exposed to lots of different microbes are less likely to develop allergies and autoimmune disorders. Bodies remember responses to viruses and bacteria, and are able to mobilise and protect us against them. Our immune systems may struggle with new, cold-causing viruses in circulation, though, meaning we will still get sick, but the immune response will still know how to fight it even after lockdowns.

There are, however, other variables to consider. Whether you are getting enough vitamin D, are stressed, or have been particularly lonely could also factor into your anti-viral response. An analysis of studies monitoring more than 300,000 people found that people who are more socially connected are 50 per cent less likely to die over a given period. Research has also shown that people with lots of social ties are even less susceptible to the common cold. Stress, which produces cortisol, also harms immune function.

Rates of colds in the UK are difficult to track; they rarely cause hospitalisations, and people are encouraged to ride them out rather than visiting their GP. However, scientists can make a good guess at what is set to hit the northern hemisphere due to patterns happening in the south. Australia has already seen a resurgence of respiratory illnesses other than Covid, as have parts of the US.

In the US, numbers of cases of respiratory syncytial virus (RSV) a type of virus that infects the lungs and commonly causes hospitalisations in children have headed upwards in recent weeks, with around 1,600 confirmed cases nationally in the week of July 17, and 2,000 the week before. In the week of 25 July a year ago there were only 11 RSV cases recorded by the Centers for Disease Control (CDC).

Similarly in Australia, a surge in RSV cases was seen in spring in states such as New South Wales and Western Australia, followed by rising rates in Queensland and Victoria. They were at an all-time low throughout the Australian winter.

The Royal Australian College of General Practitioners warned that, as in Australia, relaxing of Covid restrictions may provide an opportunity for rapid spread of RSV. Our experience should serve as a warning for paediatric hospitals in the Northern Hemisphere to ensure adequate staffing and available resources to meet the possible increased need, it wrote.

Add in pressure to attend the office even when people are feeling unwell, and youve got a recipe for transmission. A report from the ADP Research Institute showed that, during the pandemic, more than half (54 per cent) of employees globally have felt pressure from their employer to come into work at some point, even though the official line has been to stay home.

Meanwhile, the government has repeatedly encouraged a return to offices for non-essential workers in-between lockdowns, trading off trying to reignite the economy and get people back into Pret a Mangers with the risk of breathing new life into Covid caseloads.

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Your immune system is not ready for the office - Wired.co.uk