Will social distancing weaken my immune system?

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Will social distancing weaken my immune system?

In short, no.

Some worry a lack of contact with others will weaken their immune system by reducing its active contact with germs.

Some worry a lack of contact with others will weaken their immune system by reducing its active contact with germs.

But even when we're staying 6 feet from others or spending most of our time at home, our bodies are continuously responding to plenty of bacteria and other germs that inhabit indoor and outdoor environments.

US CORONAVIRUS DEATHS REACH 250,000

“We’re constantly exposed to microbes,” said Akiko Iwasaki, an immune system researcher at Yale University. "Our immune system is always being triggered.”

The effects of childhood vaccines and other built-up immunity are also long-lasting, Iwasaki said, and won't disappear overnight because we're keeping our distance from others during the pandemic.

HOW DO THE MODERNA AND PFIZER CORONAVIRUS VACCINES COMPARE?

Experts say anyone looking to boost their immune health during the pandemic should practice habits such as stress management, healthy eating, regular exercise and getting enough sleep.

CLICK HERE FOR FULL CORONAVIRUS COVERAGE

"These are the things that actually affect the immune system," Iwasaki said.

A seasonal flu shot will also help protect you from one more potential illness.

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Clinical trial finds inhaled immune response protein increases odds of recovery for hospitalised COVID-19 patients

Hospitalised COVID-19 patients in the UK who received an inhaled form of interferon beta-1a (SNG001) were more likely to recover and less likely to develop severe symptoms than patients who received a placebo, according to a new clinical trial published in The Lancet Respiratory Medicine journal. This is the first evidence published in a peer-reviewed medical journal that inhaled interferon beta-1a could lessen the clinical consequences of COVID-19 and serves as proof-of-concept that this treatment could help hospitalised patients recover, but further research is required.

As the number of COVID-19 infections continues to rise around the world, there is a pressing need to develop new treatments for the more severe and life-threatening symptoms such as pneumonia and respiratory failure.

Interferon beta is a naturally occurring protein that coordinates the body’s immune response to viral infections. Laboratory studies have found that the SARS CoV-2 virus directly suppresses the release of interferon beta, while clinical trials demonstrate decreased activity of this important protein in COVID-19 patients. The formulation of interferon beta used in this new study—SNG001—is directly delivered to the lungs via inhalation and has been trialled in the treatment of asthma and chronic obstructive pulmonary disease (COPD). This study aimed to evaluate the safety and efficacy of SNG001 to treat hospitalised COVID-19 patients.

The trial was conducted at nine UK hospitals with patients who had a confirmed SARS-CoV-2 infection. It compared the effects of SNG001 and placebo given to patients once daily for up to 14 days, and followed up patients for a maximum of 28 days after starting the treatment. Patients were recruited from March 30 to May 30, 2020, and were randomly assigned to receive the treatment or a placebo. All members of the research team were blinded to which group the patients were allocated. During the study, changes in the clinical condition of patients were monitored.

Of the 101 patients enrolled in the study, 98 patients were given the treatment in the trial (three patients withdrew from the trial) – 48 received SNG001 and 50 received a placebo. At the outset of the trial 66 (67%) patients required oxygen supplementation at baseline (29 people in the placebo group and 37 in the SNG001 group). Patients who received SNG001 were twice as likely to show an improvement in their clinical condition at day 15 or 16, compared with the placebo group.

In the placebo group, 11 (22%) of 50 patients developed severe disease (defined in this study as requiring mechanical ventilation) or died between the first dose and day 15 or 16, compared with six (13%) of 48 patients who received SNG001 (this includes three deaths in the placebo groups and none in the treatment group).

Over the 14-day treatment period, patients who received SNG001 were more than twice as likely to recover, compared to those in the placebo group—with 21 (44%) patients in the SNG001 group recovering compared with 11 (22%) patients in the placebo group (patients were deemed to have recovered when they were no longer limited in their activity). In a secondary analysis, the authors found that at 28 days, SNG001 patients were over three times more likely to recover than patients receiving placebo.

Lead author, Professor Tom Wilkinson from the University of Southampton, UK, says: “The results confirm our belief that interferon beta, a widely known drug approved for use in its injectable form for other indications, may have the potential as an inhaled drug to restore the lung’s immune response and accelerate recovery from COVID-19. Inhaled interferon beta-1a provides high, local concentrations of the immune protein, which boosts lung defences rather than targeting specific viral mechanisms. This might carry additional advantages of treating COVID-19 infection when it occurs alongside infection by another respiratory virus, such as influenza or respiratory syncytial virus (RSV) that may well be encountered in the winter months.”

The safety of inhaled interferon beta-1a was assessed by monitoring adverse events over 28 days. 26 (54%) patients in the SNG001 group and 30 (60%) patients in the placebo group had adverse events during treatment, with the most frequently reported being headache. Fewer patients in the SNG001 group had serious adverse events, compared with the placebo group.

The authors note some limitations of their study. The sample size was small and, as such, findings cannot be generalised to wider populations and healthcare settings. There were differences between the two groups at recruitment: patients in the SNG001 group had more severe disease at baseline and more patients had hypertension, and in the placebo group more patients had diabetes and cardiovascular disease. However, these factors were considered in the statistical model used, and beneficial signals for therapy were enhanced when a priori adjustments were made. Larger trials should be able to address these limitations with randomisation of more varied groups, according to the researchers.

The same research group is also assessing the effectiveness of the treatment in pre-hospital cases of COVID-19. To assess the treatment for patients who are critically ill and requiring mechanical ventilation, an alternative delivery method than the current nebuliser is needed.

Writing in a linked Comment, lead author Nathan Peiffer-Smadja (who was not involved in the study), from Assistance Publique—Hôpitaux de Paris, France, pointed out that preliminary results from the SOLIDARITY/DisCoVeRy randomised clinical trial in COVID-19 patients (which includes 8% who were mechanically ventilated) has so far failed to show efficacy of subcutaneous injectable interferon beta-1a. One potential explanation is because this route of administration doesn’t provide the targeted delivery of the drug to the lungs, which occurs with inhaled delivery. The Comment also highlights concerns that in severe COVID-19 patients the use of the drug could increase the inflammatory response and be associated with safety issues.

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Biologist uses rabies-like virus to illuminate how SARS-CoV-2 blocks immune response

Vanderbilt University researcher Yi Ren is part of an international team that has confirmed the mechanism by which SARS-CoV-2, the scientific name for the strain of coronavirus causing COVID-19, targets and impacts its host factor protein. The article “SARS-CoV-2 Orf6 hijacks Nup98 to block STAT nuclear import and antagonize interferon signaling” was published in the journal Proceedings of the National Academy of Sciences on Oct. 23.

Ren, an assistant professor of biochemistry, studies the basic mechanism by which proteins are expressed within cells, and how different viruses target and hijack the function of critical immune factors within the cells’ machinery.

Her expertise is in influenza A—the only influenza virus known to cause global flu disease epidemics—and vesicular stomatitis virus. VSV is a rabies-like virus that predominantly infects cattle, horses and pigs. The virus is highly sensitive to interferons, the signaling proteins that are made by host cells when they sense a virus. The interferons’ purpose is to induce nearby cells to boost their anti-viral defenses.

Reviewing coronavirus-related research early in 2020, Ren came upon an article that suggested the SARS-CoV-2 protein had similar characteristics to VSV, in that it acts to tamp down the interferons that would otherwise kick off an immune response in the host. “From the literature review, I understood that I had the requisite specialist knowledge of how protein expression is blocked in VSV to meaningfully contribute to COVID-related research,” Ren said.

Together with longtime collaborators at the University of Texas Southwestern Medical Center and the Icahn School of Medicine at Mount Sinai, “We were able to test the direct interaction between the host factor that I work with and the SARS-CoV-2 protein. We found that, indeed, they interact,” Ren said.

The findings show that SARS-CoV-2 uses a similar strategy as VSV to target the same susceptible protein known as a host factor. The difference is that SARS-CoV-2 has a mechanism that stops proteins from sharing genetic information with the host cell nucleus. This blocking behavior enables suppression of the immune system. This mechanistic finding was a huge surprise for Ren, who has spent so much time in the lab with VSV.

“Even though SARS-CoV-2 is an entirely new virus that the world is grappling with, it deploys a similar strategy to target the same host factor as VSV, making me feel somewhat familiar with the virus. After so many years of studying influenza A and VSV, to see such a small difference on a cellular level resulting in what we’ve seen during this pandemic puts these ‘small’ differences into perspective,” said Ren.

The lab continues to work on the structural characterization of the virus-host interaction so researchers can explore it further. Ren’s team soon will be able to show how the virus protein targets the host machinery and its consequences on the atomic level, an essential step in designing therapeutics to enable an appropriate host immune response.

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‘Multi-omics’ adds new cell to immune family tree

WEHI researchers have used powerful ‘single cell multi-omics’ technologies to discover a previously unknown ancestor of T and B lymphocytes, which are critical components of our immune system.

Using an approach akin to breaking a sports team’s performance down to the individual player statistics, the researchers looked at multiple aspects of single developing immune cells to define which cells would only give rise to T and B lymphocytes. This revealed a new stage in lymphocyte development, information which could enrich future studies of the immune system. The discovery has also led to new research opportunities, with WEHI establishing of one of Australia’s first dedicated and integrated single cell research platforms in 2018, which is now being used to solve other research questions.

The research, which was published in Nature Immunology today, was led by Dr. Shalin Naik, Dr. Daniela Zalcenstein, Mr Luyi Tian, Mr Jaring Schreuder and Ms Sara Tomei.

Focussing on single cells

Our immune system comprises many different types of cells with different functions, but all immune cells are derived from a single type of cell, a blood stem cell. The development of different immune cell types occurs through a branching ‘family tree’ of immature cells. At earlier stages of immune cell development, individual cells can give rise to several different types of mature cell, but as development progresses, cells become more limited in which final mature cells they can produce.

T and B lymphocytes—which are critical for targeted, specific immune responses—are closely related immune cells, meaning they share many common steps in their development, said Dr. Naik. “Decades of research have defined how T and B lymphocytes develop, and the ‘branch points’ in their family tree when the developing cells lose the capacity to develop into other immune cell types,” he said.

Dr. Zalcenstein said that to gain new insights into questions such as how immune cells develop, the team established Australia’s first ‘single cell multi-omics’ platform, which is now available to all researchers within the Single Cell Open Research Endeavour (SCORE) established by Dr. Naik and Dr. Zalcenstein in collaboration with Dr. Stephen Wilcox of WEHI’s Genomics Hub and Associate Professor Matthew Ritchie.

“Multi-omics technologies combine different biological data sets—such as genomics, transcriptomics and proteomics—to compare different samples in more detail than is possible by looking at one data set. We have applied this approach to study individual cells, in this case developing immune cells, to understand in more detail which cells can give rise to lymphocytes. This approach is called single cell multi-omics,” she said.

“Rather than looking at data combined from many cells in a sample, we focus in on individual cells to understand the differences that exist within a larger population. It’s like looking at a football team—you can average out the number of goals, tackles and kicks per player in a game, but if you look at individual player statistics, you may discover that one player scored lots of goals, while another player was responsible for most of the tackles,” she said.

A new lymphocyte progenitor

SCORE’s study of immune cell precursors revealed a previously unrecognised cell type that could give rise to T and B lymphocytes, but not other immune cells.

“This cell occurred much earlier in lymphocyte development than we had suspected,” Dr. Naik said. “Previous techniques had grouped different immune progenitors together, but by studying individual cells we were able to identify one cell type that was committed to developing into T and B lymphocytes.”

The discovery adds a new layer to the family tree of T and B lymphocytes and could provide a boost to other areas of research.

“Understanding in more detail how T and B lymphocytes develop could lead to better approaches to regenerate these cells as a treatment for certain diseases,” Dr. Naik said. “We also know that many types of leukaemia arise from defects in early stages of immune cell development, so we are curious to know whether this progenitor cell has links to any forms of leukaemia.”

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Immune cell activation in severe COVID-19 resembles lupus

In severe cases of COVID-19, Emory researchers have been observing an exuberant activation of immune cells, resembling acute flares of systemic lupus erythematosus (SLE), an autoimmune disease.

Their findings point towards tests that could separate some COVID-19 patients who need immune-calming therapies from others who may not. They also may begin to explain why some people infected with SARS-CoV-2 produce abundant antibodies against the virus, yet experience poor outcomes.

The results were published online on Oct. 7 in Nature Immunology.

The Emory team’s results converge with recent findings by other investigators, who found that high inflammation in COVID-19 may disrupt the formation of germinal centers, structures in lymph nodes where antibody-producing cells are trained. The Emory group observed that B cell activation is moving ahead along an “extrafollicular” pathway outside germinal centers—looking similar to they had observed in SLE.

B cells represent a library of blueprints for antibodies, which the immune system can tap to fight infection. In severe COVID-19, the immune system is, in effect, pulling library books off the shelves and throwing them into a disorganized heap.

Before the COVID-19 pandemic, co-senior author Ignacio (Iñaki) Sanz, MD and his lab were focused on studying SLE and how the disease perturbs the development of B cells.

Sanz is head of the division of rheumatology in the Department of Medicine, director of the Lowance Center for Human Immunology, and a Georgia Research Alliance Eminent Scholar. Co-senior author Frances Eun-Hyung Lee, MD is associate professor of medicine and director of Emory’s Asthma/Allergy Immunology program.

“We came in pretty unbiased,” Sanz says. “It wasn’t until the third or fourth ICU patient whose cells we analyzed, that we realized that we were seeing patterns highly reminiscent of acute flares in SLE.”

In people with SLE, B cells are abnormally activated and avoid the checks and balances that usually constrain them. That often leads to production of “autoantibodies” that react against cells in the body, causing symptoms such as fatigue, joint pain, skin rashes and kidney problems. Flares are times when the symptoms are worse.

Whether severe COVID-19 leads to autoantibody production with clinical consequences is currently under investigation by the Emory team. Sanz notes that other investigators have observed autoantibodies in the acute phase of the disease, and it will be important to understand whether long-term autoimmune responses may be related to the fatigue, joint pain and other symptoms experienced by some survivors.

“It’s an important question that we need to address through careful long-term follow-up,” he says. “Not all severe infections do this. Sepsis doesn’t look like this.”

In lupus, extrafollicular B cell responses are characteristic of African-American patients with severe disease, he adds. In the new study, the majority of patients with severe infection were African-American. It will be important to understand how underlying conditions and health-related disparities drive the intensity and quality of B cell responses in both autoimmune diseases and COVID-19, Sanz says.

The study compared 10 critically ill COVID-19 patients (4 of whom died) admitted to intensive care units at Emory hospitals to 7 people with COVID-19 who were treated as outpatients and 37 healthy controls.

People in the critically ill group tended to have higher levels of antibody-secreting cells early on their infection. In addition, the B cells and the antibodies they made displayed characteristics suggesting that the cells were being activated in an extrafollicular pathway. In particular, the cells underwent fewer mutations in their antibody genes than seen in a focused immune response, which is typically honed within germinal centers.

The Nature Immunology paper was the result of a collaboration across Emory. The co-first authors are Matthew Woodruff, Ph.D., an instructor in Sanz’s lab, and Richard Ramonell, MD, a fellow in pulmonary and critical care medicine at Emory University Hospital.

Ramonell notes that the patients studied were treated early during the COVID-19 pandemic. It was before the widespread introduction of the anti-inflammatory corticosteroid dexamethasone, which has been shown to reduce mortality.

The team’s findings could inform the debate about which COVID-19 patients should be given immunomodulatory treatments, such as dexamethasone or anti-IL-6 drugs. Patients with a greater expansion of B cells undergoing extrafollicular activation also had higher levels of inflammatory cytokines, such as IL-6.

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Fostamatinib in chronic immune thrombocytopenia: No comparison—added benefit not proven

Fostamatinib is approved for the treatment of chronic immune thrombocytopenia in adults who are refractory to other treatments (in particular to treatment with corticosteroids). The German Institute for Quality and Efficiency in Health Care (IQWiG) examined in an early benefit assessment whether fostamatinib offers an added benefit for these patients in comparison with eltrombopag or romiplostim.

The drug manufacturer recognized both drugs as appropriate comparator therapy, but presented neither direct nor indirect comparisons between fostamatinib and the appropriate comparator therapy. IQWiG therefore concluded that an added benefit is not proven.

Comparisons with appropriate comparator therapy necessary

The approval studies, the data of which the manufacturer cited in its dossier, compared fostamatinib with placebo. Randomized controlled trials with direct comparisons between fostamatinib and eltrombopag or romiplostim are not available. The manufacturer did not identify any suitable data for an adjusted indirect comparison.

Comparisons with the appropriate comparator therapy are necessary, however, to understand the benefit and harm that the different treatment options have for the patients in relation to each other. They are the backbone of the early benefit assessment: There is no other way to determine an added benefit of the drug in comparison with the current standard treatment.

G-BA decides on the extent of added benefit

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How to boost your immune system in good time for flu season

Already starting to panic about flu season? You’re not alone.

Do you need a flu jab? How can you tell the difference between flu symptoms and coronavirus? How can you boost your immune system ahead of winter?

There has been an intense focus on health and immunity this year thanks to Covid-19 and now everyone’s starting to think about how best to protect themselves for the winter.

‘The immune system is one of the most complex and comprehensive systems in the human body,’ says Mike Wakeman, a clinical pharmacist and ambassador for health food supplement CurraNZ.

‘It’s also one of the most important. It’s the invisible barrier against all sorts of foreign assaults from micro-organisms (fungal infections, bacteria and Covid-19) and allergens (pollens, dust mites and chemicals) that we encounter on a daily basis.’

Our first level of immunity is called the innate immune system and is activated as soon as a disease-causing micro-organism is detected. It can detect invaders such as viruses, bacteria, parasites and toxins and attempt to kill them off, before they can enter the body.

‘Innate immunity is made up of things like skin, the gastrointestinal tract and the respiratory tract. Inside these parts of the body are barriers like mucus, secretion and gastric acid, which try to stop the invaders getting in. The innate system also has immune cells (called macrophages), which are some of the most abundant cells in the human body and specialise in detecting and destroying bacteria and other harmful organisms by engulfing and killing them,’ says Mike.

The second level of protection is called the adaptive immune system, which is activated to enhance the innate system.

‘This is mainly cells called lymphocytes,’ explains Mike. ‘They are a type of white blood cell that have the ability to recognise a unique part of a micro-organism, memorise it and produce specific pathogen-neutralising compounds known as immunoglobulins. So when the body encounters this particular antigen [foreign substance] again it can produce more of the immunoglobulins it knows can kill it. This is the basis of how immunisations and flu jabs work.’

Generally, our immune system does an amazing job of defending us but a recent review in the Journal of Sport and Health Science found that ageing, obesity, and inactivity have a negative effect on the immune system.

‘The idea of boosting your immunity sounds like a simple enough process, but it’s not like giving yourself an injection or taking a shot,’ says Mike.

‘You need to think more about optimising your immunity on a daily basis as some vitamins and minerals take longer to generate their effect than others. Vitamin C is water soluble so absorbed straight away, while vitamin D is fat-soluble so is stored in fat cells rather than circulating in the body.

‘Autumn is the best time to think about how to build up immunity for winter and a good quality multi-vitamin is a cheap way to start optimising your protection.’

Spot the signs of a weakened immune system

Don’t wait until you become poorly to start looking after yourself – if you are suffering from any of these problems it’s worth taking stock and taking some extra care, says Mike.

Spot the signs

Cracks in the corner of the mouth

‘This can indicate some aspects of the immune system might be under stress. Vitamins and minerals are vital as they can help to resolve minor issues like this.’

Constant cold symptoms or infection

‘Constant and repeated colds are not only a sign of a weakened immune system, but also place extra demands on immune micronutrient status.’

Wounds take longer to heal

‘Poor healing is a typical symptom of a challenged immune system, and a number of vitamins, such as vitamin C can help improve the skin function.’

Bleeding gums

‘Often poor oral hygiene can be a major challenge to the immune system, so brush your teeth regularly, twice daily and don’t forget to floss.’

Constantly tired and over-stressed

‘Stress can really impact on our immune function, so take time out to look after yourself, get some exercise and relieve stress and exhaustion as much as possible.’

A weakened immune system can be helped with simple diet changes. ‘Most of us are deficient in vitamin D which is produced by the body when we’re exposed to sunshine,’ says Mike.

‘We don’t get enough of it during the summer and definitely not in winter. Oily fish, like pilchards, sardines, mackerel and some salmon are a good source of vitamin D and also high in omega-3 fatty acids, which may also help enhance the function of the immune cells.’

Mike is keen to emphasise that lots of what you need to bolster the immune system can be found in food. ‘You should be eating at least five portions of fruit and veg a day,’ he says.

‘Not only do vitamins and minerals optimise the immune system, they have an anti-inflammatory effect too, so if the immune system over-responds, these micronutrients can help resolve the inflammation this causes. These vitamins and minerals also help the body produce anti-bacterial compounds that fight infection within the body while compounds known as polyphenols support immunity.’

So, a healthy diet has never been more important. When teamed with a good quality multi-vitamin you should stand a better chance of fighting off the winter nasties.

Supplements to help boost your immune system

Five of the best supplements to give a helping hand

1. Extra special

Vitabiotics Immunace Extra Protection contain lycopene, resveratrol, astaxanthin, alpha lipoic acid and vit D. £10.15 (30 tablets)

2. Gum deal

Sambucol ImmunoForte Gummies contain black elderberry flavonoids, plus vitamin C, zinc and high levels of antioxidants. Suitable for vegans. £11 (30 gummies)

3. Vit blitz

Urgent-C Everyday Immune Support contains 1,000mg of vitamin C, plus vitamin D, zinc, selenium, beta glucans and elderberry extract which all help the normal function of the immune system. £14.95 (30 sachets)

4. Berry nice

Blackcurrants offer anti-viral and anti-microbial properties to help the body ward off infection. A single capsule of CurraNZ is equivalent to a handful of berries. £21.75 (30 capsules)

5. Sweet Treat

Made with all-natural ingredients and boosted with 100 per cent NRV vitamin D, C and B12, these new Perkier +Immune bars are tasty plant-based snacks to boost immune health. £15.99 (15 bars)

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Memory training for the immune system

After an infection of the human body with a pathogen, a cascade of reactions will usually be set into motion. Amongst others, specific cells of the immune system known as T cells get activated in the lymph node and will subsequently divide and proliferate.

At the same time, these cells will gain certain functions, that enable them to destroy other cells, that are e.g. infected by a virus. In addition, they produce certain proteins—so called cytokines—with which they can stop the reproduction of the pathogen.

The immune system and its function are the main focus of the research of Professor Wolfgang Kastenmueller, director of the Chair of Systems Immunology I at the Institute of Systems Immunology of the Julius-Maximiliams-Universität Würzburg (JMU). Together with Professor Georg Gasteiger, director of the Chair of Systems Immunology II, they lead the Max-Planck Research group of Systems Immunology.

Their research focus is the interaction of the immune system with the organism, especially the interaction of different cells of the immune system within local networks and with other cells of other organ systems.

Recently Kastenmueller and his team deciphered new details of the functioning of the immune system, which are important for the immune system to remember recent infections. Their results have been published in the latest issue of the scientific journal Nature Immunology. Their findings could help to improve immune therapy towards tumor diseases.

“If a body has fought and eliminated a pathogen successfully, most of the recently proliferated T cells are no longer needed and will die,” Wolfgang Kastenmueller explains. But about five to ten percent of these cells survive and develop into a long lasting “memory population,” that will protect the body against future infections.

Improvement of the immunological memory

Kastenmueller describes the main result of his study, “In our recent work we identified a transcription factor—BATF3, that very specifically regulates the survival of these cells and therefore the transition into a memory response.” The scientists could show that this factor only gets produced shortly after the initial activation of T cells. The absence of this factor leads to a permanent malfunction of the memory response.

Until now the role of this factor for so-called CD8+ T cells was unclear. It was only after the scientists overexpressed this factor in CD8+ T cells that the importance became clear, as they could see that the survival of these cells and thus the immunological memory improved significantly.

This study was conducted in close collaboration with the Medical Clinic II of the University clinic of Wuerzburg. It combines basic research with applied medicine and could help to develop better therapies for cancer treatments that use the immune system of the patient—so-called CAR-T cell therapy.

Using CAR-T cell therapy, T cells get extracted from the blood of the patient and are subsequently genetically modified with the chimeric antigen receptor (CAR) molecules. This modification enables T cells to attack tumor cells, which they couldn’t biochemically detect before. These modified T cells are subsequently transferred back into the patient.

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New connections reveal how cancer evades the immune system

If cancer is a series of puzzles, a new study pieces together how several of those puzzles connect to form a bigger picture.

One major piece is the immune system and the question of why certain immune cells stop doing their job. Another piece involves how histones are altered within immune cells. A third piece is how a cell’s metabolism processes amino acids.

“Nobody knew if those questions were all connected. We were able to place several of these puzzles together and see how it works,” says Weiping Zou, M.D., Ph.D., Charles B. de Nancrede and a Professor of Surgery, Pathology, Immunology and Biology at the University of Michigan and director of the Center of Excellence for Immunology and Immunotherapy at the U-M Rogel Cancer Center.

Zou is senior author on a paper published in Nature that includes multiple labs from the Rogel Cancer Center and collaborators from Poland.

The study found a connection between these three separate puzzles that suggests targeting the amino acid methionine transporter in tumor cells could make immunotherapy effective against more cancers.

It starts with T cells, the soldiers of the immune system. Cancer can turn these cells abnormal, preventing T cells from mounting an attack against it. The question is: what causes this?

Researchers looked at the tumor microenvironment, specifically how tumors metabolize amino acids. They found an amino acid called methionine had the most impact on T cell survival and function. T cells with low levels of methionine became abnormal. Low methionine in the T cells also altered histone patterns that caused T cells to be impaired.

Introducing tumor cells to the picture creates a fight between the tumor cells and the T cells for methionine. Over and over, the tumor cells win, taking the methionine from the T cells and rendering them ineffective.

Previous research has considered a systemic approach to starve tumor cells of methionine, with the idea that the tumor cells are addicted to it. But, Zou says, this study shows why that approach may be a double-edged sword.

“You have competition between tumor cells and T cells for methionine. The T cells also need it. If you starve the tumor cells of methionine, the T cells don’t get it either. You want to selectively delete the methionine for the tumor cells and not for the T cells,” Zou says.

In fact, the study found that supplementing methionine actually restored T cell function. High enough levels of methionine meant there was enough for both tumor cells and T cells.

One key is that tumor cells have more of the transporters that deliver methionine. The researchers found that impairing those transporters resulted in healthier T cells as the T cells could compete for methionine.

Zou was awarded a $3.2 million grant from the National Cancer Institute to advance this work.

“There are still a lot of mechanistic details we have not worked out, particularly the detailed metabolic pathways of methionine metabolism. We also need to understand how metabolism pathways may be different from tumor cells and T cells. We hope to find a target that is relatively specific to tumor cells so that we do not harm the T cells but impact the tumor,” Zou says. This work will be the focus of the new grant.

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Naked mole rats have tumor-fighting immune systems

Could naked mole rats help cure cancer? Scientists discover the rodents have special tumor-fighting immune systems

  • Until recently, it was believed naked mole-rats had healthy cells that were resistant to being converted into cancer cells
  • Researchers injected the cells with cancer-causing genes that usually cause tumors in mice 
  • The genes that cause cancer in other rodent cells also caused naked mole-rat cells to become cancerous
  • This suggests the cells and molecules that surround naked mole rat cells prevent other cells from turning into tumors

Naked mole-rats have special tumor-fighting immune systems that make them resistant to cancer, a new study suggests.

It was previously believed that the animals had cells that were resistant to being converted into cancer cells.

But researchers have now discovered that the environment of the naked mole-rat’s body prevents the cancer from developing, not a feature of the rodent’s cells that prevent them from becoming cancerous. 

The team, from the University of Cambridge, says understanding naked mole-rats’ resistance to cancer can help us understanding the early stages of cancer and how to treat it.  

A new study has found that  the cells and molecules that surround naked mole rat cells prevent other cells from turning into tumors (file image)

Naked mole-rats, also known sand puppies, are burrowing rodents that are native to parts of East Africa.

They have other unique traits such as not being able to feel certain types of pain and being able to survive for along time with low levels of oxygen.  

It can live a long time for an animal of its size, up to 32 years, and is highly resistant to cancer and its related tumors. 

Until recently, it was believed naked mole-rats almost never got cancer because their healthy cells were impervious to being converted into cancer cells. 

But now, it’s believed that the rodents’ bodies can actually stop cancer cells from multiplying and spreading.

For the study, published in the journal Nature, the team looked at 79 different cell lines grown from five different types of tissues.

They grew the cells of the intestines, kidneys, lungs, pancreases and skin of 11 individual naked mole-rats. 

Next, researchers infected the cells with altered viruses so that the cells would develop cancer-causing genes. 

The genes caused cancerous tumors when injected in mice and rats cells.

However, the genetically altered naked mole rat cells also began to copy itself and spread. 

‘To our surprise, the infected naked mole-rat cells began to multiply and rapidly form colonies in the lab,’ said lead researcher Dr Fazal Hadi, a professor from the Cancer Research UK Cambridge Center.

‘We knew from this accelerated growth that they had become cancerous.’   

This means the genes that cause cancer in other rodent cells also caused naked mole-rat cells to become cancerous. 

This finding suggests that the cells and molecules that surround other naked mole rat cells prevent them from turning into tumors. 

‘The results were a surprise to us and have completely transformed our understanding of cancer resistance in naked mole-rats,’ said co-senior author Dr Walid Khaled a professor in the department of pharmacology at the University of Cambridge.  

‘If we can understand what’s special about these animals’ immune systems and how they protect them from cancer, we may be able to develop interventions to prevent the disease in people.’  

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