T-Cells Archives - Amazing Health Advances

Curbing Candida: The Cells That Keep Fungal Infections at Bay

AHA Publisher — Thu, 14 Jul 2022 07:00:19 +0000

Weizmann Institute of Science via Newswise – Of all the fungi that live in the human body, the most infamous is probably the yeast Candida. This distant cousin of baker’s yeast is notorious for causing various types of thrush that can be a major nuisance, but it can also lead to an invasive infection that may, on occasion, prove fatal. In a study published today in Nature Immunology, a Weizmann Institute of Science research team headed by Prof. Jakub Abramson uncovered a previously unknown defense mechanism employed by the immune system in fighting Candida infections. Candida is present at low levels in the bodies of most healthy people, forming part of the microbiome – a diverse spectrum of microbes that reside peacefully in our gut and on our skin. Under normal circumstances, Candida is held in check by the immune system, but it can occasionally grow excessively, invading the lining of the mouth, the vagina, the skin or other parts of the body. In severe cases, it can spread to the bloodstream and from there to the kidneys. Such life-threating infections may occur when a person’s immune system has been weakened, for example, by AIDS or by immunosuppressive drugs such as cancer chemotherapy or steroids. Antibiotics, which wipe out many of the beneficial bacteria within our microbiome, can also unleash local or invasive Candida eruptions by providing this yeast with an unfair advantage vis-à-vis other microorganisms. That’s why, for instance, women sometimes develop a vaginal yeast infection after taking antibiotics. Until now, the immune cells that got most of the credit for defending the body against Candida were the small, round lymphocytes of the T cell type, called TH17. These cells were also the ones to take the blame when this defense failed. In the new study, postdoctoral fellow Dr. Jan Dobeš, working together with colleagues in Abramson’s lab in Weizmann’s Immunology and Regenerative Biology Department, discovered that a powerful commando unit of TH17 cells capable of fighting Candida cannot be generated without crucial early support from an entirely different contingent: a subset of rare lymphoid cells known as type-3 innate lymphoid cells, or ILC3, that express a gene called the autoimmune regulator, or Aire The two groups of cells belong to the two different arms of the immune system, which, like foot patrols and specialized units, join forces against a common enemy. The Aire-ILC3s – part of the more ancient, innate arm – spring into action almost immediately upon encountering a threat – in this case, a Candida infection. The TH17s belong to the immune system’s more recent, adaptive arm, which takes several days or even weeks to respond, but which launches a much more targeted and potent attack than the innate one. The scientists found that as soon as Candida starts infecting tissues, the Aire-ILC3s engulf the yeast whole, chop them up and display some of the yeast pieces on their surfaces. That’s how these bits are presented to the TH17s, a few of which are generally on call in the lymph nodes, ready for an infection alert. This kind of presentation instructs the specialized T cells to start dividing rapidly, soaring in number from a few lone commandos to several hundred or even thousands of Candida-specific fighters, capable of destroying the yeast at the sites of infection. “We have identified a previously unrecognized immune system weapon that is indispensable for orchestrating an effective response against the fungal infection,” Abramson says. Abramson became intrigued by Candida because it commonly leads to severe, chronic infections in people with a rare autoimmune syndrome caused by defects in the Aire gene. Abramson’s lab had conducted extensive studies of this gene, helping to clarify its role in preventing autoimmune disorders. That research, as well as studies by other scientists, had shown that Aire-expressing cells in the thymus instruct developing T cells to refrain from attacking the body’s own tissues. When Aire is defective, T cells fail to receive proper instructions, consequently causing widespread autoimmunity that wreaks havoc in multiple body organs. But one puzzle remained: Why would Aire-deficient patients suffering from a devastating autoimmune syndrome also develop chronic Candida infections? While trying to complete the Aire puzzle, Dobeš and colleagues found that outside the thymus, Aire is also expressed in a small subset of ILC3s in the lymph nodes. The researchers then genetically engineered two groups of mice: One lacked Aire in the thymus, and the other group lacked it in the ILC3s in the lymph nodes. The first group developed autoimmunity but was able to successfully fight off Candida. In contrast, those in the second group, the ones lacking Aire in ILC3s, did not suffer from autoimmunity, but were unable to generate numerous Candida-specific TH17s. Consequently, they failed to effectively eliminate Candida infections. In other words, without Aire-expressing ILC3s, the specialized T cells needed for fighting Candida were not produced in sufficient numbers. “We found an entirely new role for Aire, one that it plays in the lymph nodes – turning on a mechanism that increases the numbers of Candida-fighting T cells,” Dobeš explains. These findings open up new directions of research that in the future may help develop new treatments for severe Candida, and possibly for other fungal infections. The newly discovered mechanism might, for example, help produce large numbers of Candida-fighting T cells to be used in cell therapy. And if scientists one day identify the signals by which Aire-ILC3s boost T cell proliferation, these signals themselves might provide the basis for new therapies. Study participants also included Osher Ben-Nun, Amit Binyamin, Dr. Yael Goldfarb, Dr. Noam Kadouri, Yael Gruper, Tal Givony and Itay Zalayat of Weizmann‘s Immunology and Regenerative Biology Department; Dr. Liat Stoler-Barak and Prof. Ziv Shulman of the Systems Immunology Department; Katarína Kováčová, Helena Böhmová and Evgeny Valter of Charles University, Prague; Bergithe E. Oftedal and Prof. Eystein S. Husebye of the University of Bergen, Norway; and Dr. Dominik Filipp of the Institute of Molecular Genetics of the Czech Academy of Sciences, Prague. To read the original article click here.

The post Curbing Candida: The Cells That Keep Fungal Infections at Bay appeared first on Amazing Health Advances.

New Cancer Treatment Fools the Immune System to Attack

AHA Publisher — Wed, 06 Jul 2022 07:00:48 +0000

Brian Blum via Israel21c – Immunotherapy holds perhaps the greatest promise for fighting cancer in the 21st century. Rather than bombarding the body with toxic chemicals, as in chemotherapy, immunotherapy utilizes the immune system to neutralize malignant tumors. The only problem: It only works in about 20 percent of patients with solid tumors. The reason is straightforward, but still represents a vexing roadblock for cancer researchers: Tumors are not an infection coming from outside but an internal malfunction of the body’s own cells, which begin to replicate out of control. “Cancer looks like us. It’s hard for the immune system to identify,” explains Dr. Asher Nathan, CEO of NeoTX, a Rehovot-based startup developing a novel way of knocking out tumors – by coating them in bacteria. “Unlike with cancer, our bodies are finely tuned to attack bacteria,” Nathan says. “Bacteria is a billion years old. Our immune systems have had a long time to figure out how to effectively neutralize bacterial infections. That’s why you don’t wake up in the morning with a cold and think, ‘I’m going to die.’” Cancer, of course, is a very different story. Compared with bacteria, “cancerous tumors are like the new kid on the block,” Nathan notes. NeoTX is not Nathan’s first foray into medical technology; after immigrating to Israel 40 years ago from Chicago, he founded IntelliGene and EvoRX, two biotech companies formed around technologies he invented. For NeoTX, Nathan identified and licensed a drug developed by the Swedish company Active Biotech called naptumomab estafenatox (NAP). NAP is composed of two proteins: a genetically modified “superantigen” and an antibody that latches onto a tumor via a molecule called 5T4 found primarily on tumors. A superantigen is a bacterial derivative that elicits a strong antibacterial immune response. NeoTX calls its technology “Tumor-Targeted Superantigen” or TTS. Once NAP’s 5T4 antibody has attached itself to a tumor, the superantigen “reprograms” the immune system to mount an antibacterial response against the bacteria as well as the tumor. “The concept behind this drug is, let’s coat the tumor with a bacterial molecule so that the immune system will go into ‘Defcon 1’ and attack the tumor as if it’s bacteria,” Nathan says. The Secret Weapon Once the immune system knows what to look for, it sends in the body’s secret weapon: killer T-cells. The T-cells identify the bacteria-coated tumors, then start to create an army of cells primed to attack any superantigens they find. Nathan recommends the video below to see how T-cells work; they “grope around like a blind robot” and after hitting a superantigen, punch a hole in the cell … then insert a molecule that causes the cell to explode.” It’s a fine balance. When fighting a bacterial infection, “the body can go crazy,” Nathan notes. “You can get a high fever that exhausts the immune system. That’s how the bacteria continue to fight. We genetically engineered our superantigen to be safer. It doesn’t generate as strong a response, but it still creates a very powerful immune reaction.” Targeting bacteria is smart for another reason: Part of how tumors succeed in evading the body’s defenses is by releasing chemicals that weaken the immune response. “Anything we do nearby the tumor becomes problematic,” Nathan says. But with NAP, “the tumor-killing T-cells are created far from the immune-suppressed tumor site.” Only then do they begin their journey to seek out and destroy the tumors. Moreover, when the immune system encounters a superantigen bound to a tumor, it modifies the suppressive micro-environment around the tumor so that the body’s natural defenses are better able to kill it. “This creates a natural, holistic and profound immune response,” Nathan says. Reboots the Immune System But the best may be yet to come. “When we’ve tested this drug in animals, we find that even when you try to reintroduce cancers into, say, a mouse that’s been cured by the technology, it doesn’t stick,” Nathan says. “None of the mice that were ‘rechallenged’ got cancer again. The drug ‘wakes up’ the immune system – at least in mice – and we don’t need any more drug.” Nathan likens it to the reboot function on a computer. “The drug reboots the immune system so it can do what it natively needs to do – remove the suppressive environment and kill as many tumor cells as possible. Then, the T-cells can go after more targets.” NeoTX’s bacterial coating approach is currently in a Phase I trial in Israel and, based on encouraging results, has begun a Phase 2 trial in the United States with 30 patients. One patient has non-small cell lung cancer that had metastasized to the liver. “That’s a death sentence, usually within four months,” Nathan says. The patient received NeoTX’s drug over a decade ago (prior to it being licensed from Active Biotech). “She lived for 11 years and died of something else, not her cancer.” NAP plays particularly well with checkpoint inhibitors, another type of cancer treatment that aims to tamp down “checkpoints” created by the cancer that essentially trick the T-cells into thinking the tumor is a friend. “It’s like a secret handshake in a college fraternity,” Nathan quips. If the handshake were inhibited, so to speak, the T-cells would see the tumor for what it is – very much not a friend – and could attack. Combining NAP with a checkpoint inhibitor “allows our drug to kill more tumor cells,” Nathan says. AstraZeneca Collaboration Pharma giant AstraZeneca is collaborating with NeoTX on the former’s own checkpoint inhibitor technology. The hope is that patients who don’t normally respond will have greater success in beating back their cancers. Developing and commercializing any new drug can take up to 15 years and many millions of dollars. NeoTX has raised around $80 million so far. Nathan is optimistic that if NAP passes Phase 2 and 3 trials, it could hit the market as early as 2027. While the technology has so far been tested on solid lung, esophageal and urethral cancer tumors, patients with blood cancer such as lymphoma and leukemia could benefit, too – in particular those who are candidates for CAR-T, a promising treatment that involves removing T-cells from a patient, engineering them for maximum killing ability in a lab, then reinjecting them. CAR-T, a form of immunotherapy, tends to work well for blood cancers but poorly for solid tumors. That’s another aim for NeoTX – to provide a pharmaceutical complement that will allow CAR-T to be effective outside the blood cancer domain. Immunotherapy has become a crowded field. “If you look at all the companies that are trying to elicit an immune system response, there are probably 1,000 out there. But for the specific mechanism we’re trying, it’s zero,” Nathan notes. “One of our investors said to us, ‘You’re either geniuses or you’re crazy.’ I replied, ‘What makes you think it’s one or the other?’” NeoTX has no shortage of geniuses. Roger Kornberg, the 2006 winner of the Nobel Prize in chemistry, is the company’s chief scientist (as well as a long-time collaborator with Nathan in his previous endeavors). Michael Levitt and Arieh Warshel, who shared a Nobel in chemistry in 2013, are advisers. Dr. Marcel Rozencweig, a medical oncologist and 18-year veteran of pharma company Bristol Myers Squibb, where he was head of global oncology, is NeoTX’s president. Recently, the head of global clinical oncology at Bayer pharmaceuticals, Dr. Scott Fields, joined NeoTX as chief medical officer. “It is extremely rare that someone as high up as Scott Fields would leave pharma to work in such a small company,” Nathan tells ISRAEL21c. “It is even more rare that he would come to a company based in Israel.” Cancer, sadly, isn’t going away anytime soon. “The average person develops around five cancerous or pre-cancerous cells a day,” Nathan notes. “Our bodies are very efficient at killing, such that most people don’t get a new cancer every day. Our drug could level the playing field so the body can do what it’s meant to.” For more information, click here To read the original article click here.

The post New Cancer Treatment Fools the Immune System to Attack appeared first on Amazing Health Advances.

Researchers Identify, Test Novel Drug That May Stop Heart Failure Progression

AHA Publisher — Fri, 24 Jun 2022 07:00:10 +0000

Ohio State University Wexner Medical Center via Newswise – COLUMBUS, Ohio – Researchers at The Ohio State University Wexner Medical Center and College of Medicine have developed a novel drug molecule that targets T-cells causing inflammation in heart failure patients, stopping further progression of the disease. During heart failure, T-cells, which are part of the immune system, go from protecting the body from infection to causing heart failure to progress. In a study of heart failure mice, Ohio State University researchers found these “bad” T-cells have increased levels of a protein called estrogen receptor alpha. With the help of the Drug Development Institute, which is part of The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute, researchers identified and tested a new drug molecule that activates estrogen receptor beta, which is known to have an opposite effect of estrogen receptor alpha. The novel treatment stopped progression of heart failure. Research results were published today in the American Heart Association journal Circulation Heart Failure. “This is a major finding since we have not had a new drug developed for heart failure in the last several years. We know inflammation plays an important role in worsening symptoms of heart failure, but we have not been able to identify suitable treatments that can target ‘bad’ inflammation without affecting ‘good’ inflammation. With this drug, we can selectively target ‘bad’ T-cells and stop the disease from getting worse,” said Shyam S. Bansal, an assistant professor in the Department of Physiology and Cell Biology and an investigator at the Dorothy M. Davis Heart and Lung Research Institute. Heart failure causes chronic inflammation and affects about 6 million Americans with many needing a heart transplant, according to the American Heart Association. The two most common causes are high blood pressure and coronary artery disease. “Currently there is no treatment that can stop progression of heart failure. About half of patients die within the first five years of their diagnosis. This novel treatment addresses one of the underlying mechanisms of the disease. With this drug, we may be able to significantly improve the lifespan of patients, and if we stop the disease at an early stage, patients may not even need a heart transplant,” Bansal said. Ohio State University has patented the drug molecule, OSU-ERb-012. Future research plans are to determine the effectiveness of the drug in other animal trials, identify the lowest therapeutic dose and eventually conduct clinical trials in human heart failure patients. The research is funded by the National Institutes of Health’s Heart, Lung and Blood Institute and Ohio State’s Drug Development Institute. The studies were mostly conducted by Rachel Rosenzweig and Vinay Kumar under the supervision of Bansal. To read the original article click here.

The post Researchers Identify, Test Novel Drug That May Stop Heart Failure Progression appeared first on Amazing Health Advances.

Leukemia Cure? Patient Still Cancer-Free 11 Years After Innovative Treatment

AHA Publisher — Wed, 15 Jun 2022 08:22:07 +0000

Lorie Johnson via CBN News – Doug Olson may be 75 years old, but he feels great. He’s still cancer-free 11 years after he potentially faced death from a blood cancer called chronic lymphocytic leukemia. At that time, his doctors informed him that the treatments he had been trying we not working. “Terrified is probably the best word to describe it,” Olson told CBNNews. Feeling he had nothing to lose, Doug agreed to an experimental treatment developed at the University of Pennsylvania called CAR-T therapy. It uses the patient’s own immune system, specifically the T-cells. Olson said the process of gathering those cells took about three hours. “Your blood comes out of one arm, goes into a machine that takes out your white cells and then the rest of your blood goes back in the other arm,” he said. Scientists then take the cells they removed and add receptors to them that allow the cells to bind to invading cancer cells and kill them. These modified T-cells are then multiplied in a lab and then infused into the patient. “We used my own white cells to kill the cancer cells, but it was brand new, they’d never done it before in humans,” Olson explained. “I’m sort of an eternal optimist. I figured what the heck, it worked in mice, maybe it’ll work in me.” Indeed it did. Just five weeks after receiving the treatment, Doug’s doctor announced good news. “He said, ‘Doug, we can’t find a single cancer cell on your body,'” Olson recalled. His success paved the way for thousands to be treated with CAR-T therapy. Now, more than a decade after being one of the first patients to try the therapy, Olson is still cancer-free, a remission so remarkable it was highlighted in the medical journal Nature. “We feel pretty good about using the word, ‘cure’ now,” Olson said. The U.S. Food and Drug Administration has approved CAR-T therapies to treat blood cancers like lymphomas and leukemias as well as multiple myeloma. Ahmed Galal, MD, FRACP, MSc, is a cellular therapy specialist, hematologic oncologist, and hematologist at Duke Blood Cancer Center in Durham, North Carolina, who treats patients with CAR-T therapy. “Basically it’s a game-changer,” he told CBN News. Dr. Galal said CAR-T therapy is usually administered at academic medical centers, like Duke, after other treatments failed. He said patient results are pleasing. “Their outcome is about 45-percent for five years. Now, these are the latest studies showing the duration of response is actually extending and is not coming down,” he said. “So I think eventually this will be a cure.” While CAR-T therapy has proven successful for certain types of blood cancers, it has not shown to be effective against other more common cancers, but that could change. Cancer researchers are currently conducting trials to treat some of the deadliest forms of the disease including pancreatic and lung cancers as well as brain tumors. “This is only the start,” said Dr. Galal. “CAR-T will expand more and more to different indications including more leukemias including actually other types of cancer in the solid tumor.” So while cancer is America’s second leading cause of death behind heart disease, cancer deaths have actually fallen by more than 30 percent since 1991. Health experts say the decreased death rate is due to better prevention, such as not smoking, increased screenings, like mammograms, and treatments, such as CAR-T therapy. To read the original article click here.

The post Leukemia Cure? Patient Still Cancer-Free 11 Years After Innovative Treatment appeared first on Amazing Health Advances.

Asthma May Reduce Risk of Brain Tumors — But How?

AHA Publisher — Mon, 13 Dec 2021 08:00:44 +0000

Washington University in St. Louis via Newswise – There’s not much good that can be said about asthma, a breathing disease in which the airways become narrowed and inflamed. But there’s this: People with asthma seem to be less likely to develop brain tumors than others. And now, researchers at Washington University School of Medicine in St. Louis believe they have discovered why. It comes down to the behavior of T cells, a type of immune cell. When a person — or a mouse — develops asthma, their T cells become activated. In a new mouse study, researchers discovered that asthma causes the T cells to behave in a way that induces lung inflammation but prevents the growth of brain tumors. What’s bad news for the airways may be good news for the brain. The findings, available online in Nature Communications, suggest that reprogramming T cells in brain tumor patients to act more like T cells in asthma patients could be a new approach to treating brain tumors. “Of course, we’re not going to start inducing asthma in anyone; asthma can be a lethal disease,” said senior author David H. Gutmann, MD, PhD, the Donald O. Schnuck Family Professor of Neurology. “But what if we could trick the T cells into thinking they’re asthma T cells when they enter the brain, so they no longer support brain tumor formation and growth? These findings open the door to new kinds of therapies targeting T cells and their interactions with cells in the brain.” The idea that people with inflammatory diseases, such as asthma or eczema, are less prone to developing brain tumors was first proposed more than 15 years ago, based on epidemiologic observations. But there was no obvious reason why the two very different kinds of diseases would be linked, and some scientists questioned whether the association was real. Gutmann is an expert on neurofibromatosis (NF), a set of complex genetic disorders that cause tumors to grow on nerves in the brain and throughout the body. Children with NF type 1 (NF1) can develop a kind of brain tumor known as an optic pathway glioma. These tumors grow within the optic nerves, which carries messages between the eyes and the brain. Gutmann, director of the Washington University NF Center, noted an inverse association between asthma and brain tumors among his patients more than five years ago but didn’t know what to make of it. It wasn’t until more recent studies from his lab began to reveal the crucial role that immune cells play in the development of optic pathway gliomas that he began to wonder whether immune cells could account for the association between asthma and brain tumors. Jit Chatterjee, PhD, a postdoctoral researcher and the paper’s first author, took on the challenge of investigating the association. Working with co-author Michael J. Holtzman, MD, the Selma and Herman Seldin Professor of Medicine and director of the Division of Pulmonary & Critical Care Medicine, Chatterjee studied mice genetically modified to carry a mutation in their NF1 genes and form optic pathway gliomas by 3 months of age. Chatterjee exposed groups of mice to irritants that induce asthma at age 4 weeks to 6 weeks, and treated a control group with saltwater for comparison. Then, he checked for optic pathway gliomas at 3 months and 6 months of age. The mice with asthma did not form these brain tumors. Further experiments revealed that inducing asthma in tumor-prone mice changes the behavior of their T cells. After the mice developed asthma, their T cells began secreting a protein called decorin that is well-known to asthma researchers. In the airways, decorin is a problem. It acts on the tissues that line the airways and exacerbates asthma symptoms. But in the brain, Chatterjee and Gutmann discovered, decorin is beneficial. There, the protein acts on immune cells known as microglia and blocks their activation by interfering with the NFkappaB activation pathway. Activated microglia promote the growth and development of brain tumors. Treatment with either decorin or caffeic acid phenethyl ester (CAPE), a compound that inhibits the NFkappaB activation pathway, protected mice with NF1 mutations from developing optic pathway gliomas. The findings suggest that blocking microglial activation may be a potentially useful therapeutic approach for brain tumors. “The most exciting part of this is that it shows that there is a normal communication between T cells in the body and the cells in the brain that support optic pathway glioma formation and growth,” said Gutmann, who is also a professor of genetics, of neurosurgery and of pediatrics. “The next step for us is to see whether this is also true for other kinds of brain tumors. We’re also investigating the role of eczema and early-childhood infections, because they both involve T cells. As we understand this communication between T cells and the cells that promote brain tumors better, we’ll start finding more opportunities to develop clever therapeutics to intervene in the process.” To read the original article click here.

The post Asthma May Reduce Risk of Brain Tumors — But How? appeared first on Amazing Health Advances.

New Study Offers Possible Immunotherapy Breakthrough for Cancer

AHA Publisher — Mon, 25 Oct 2021 07:00:40 +0000

Jon Schiller via Israel21c – For cancer immunotherapy to be most effective, a patient’s immune system must be able to “see” the tumor in question. “Hotspots” on cancer cells’ outer membranes can provide this service. These molecular structures contain mutated peptides called neoantigens that the immune system’s T cells recognize as foreign – the first step in binding to the neoantigens and killing the cancerous cells. But only a handful of neoantigens qualify as hotspots. And they are hard to find because they are presented to the immune system by protein complexes that come in thousands of versions. The Weizmann Institute of Science’s Prof. Yardena Samuels and her PhD student Aviyah Peri led a team using bioinformatics to develop a method for identifying features common to many tumors. This can help develop effective immunotherapy for entire groups of patients. Their findings were published in the Journal of Clinical Investigation. The scientists applied algorithms to search through international databases of the genomes of thousands of cancer patients. Focusing on melanoma, the main cancer type studied by the Samuels lab, they looked for common mutations presented by common protein complexes. The search produced several neoantigens that could potentially be considered hotspots. Next, the scientists subjected these candidate molecules to laboratory analysis and investigated their interactions with T cells. Using this approach, the scientists identified a hotspot neoantigen derived from an oncogene known as RAS, which is involved in a third of all human cancers and 20% of melanoma cases. They and their colleagues isolated the T cell receptor that can recognize this hotspot neoantigen in melanoma tumors. They then engineered T cells from healthy individuals to express this receptor and incubated them with tumor samples from patients whose tumors displayed this hotspot. The T cells killed only those cells that displayed the neoantigen. “We’ve uncovered a neoantigen that is expressed in thousands of new melanoma cases every year, and we’ve shown that it can be used in these patients to mark tumor cells for immune destruction,” Peri said. “Our study suggests that our newly developed platform can lead to ‘off-the-shelf’ immunotherapies in which T cell receptors that recognize cancer hotspots can be prepared in advance, ready to be applied in groups of patients whose tumors have been shown to harbor these hotspots,” said Samuels. Also participating in the study were the late Prof. Nir Friedman of Weizmann’s Immunology Department, Prof. Masha Y. Niv of the Hebrew University of Jerusalem, Prof. Steven A. Rosenberg of the US National Cancer Institute, Prof. Cyrille J. Cohen of Bar-Ilan University, Dr. Ansuman T. Satpathy of Stanford University School of Medicine and other researchers. To read the original article click here.

The post New Study Offers Possible Immunotherapy Breakthrough for Cancer appeared first on Amazing Health Advances.

White Blood Cells May Be Harnessed to Boost Cancer Immunotherapy

AHA Publisher — Tue, 12 Oct 2021 07:00:00 +0000

Jon Schiller via Israel21c – White blood cells called Eosinophils can be “summoned” in order to fight cancer by both destroying the cancer cells directly as well as recruiting the immune system’s cancer-fighting T-cells, according to a new study published in the journal of the American Association for Cancer Research. Eosinophils produce powerful destructive proteins intended for fighting parasites. However, in the modern Western world, where high levels of hygiene have significantly reduced the risk of many parasites, eosinophils can be harmful, inducing allergies and asthma. Considering the destructive power of eosinophils, the researchers decided to test the potential benefits of these white blood cells if turned against cancer cells. Examining tissue samples of lung metastases taken from breast cancer patients, the researchers found that eosinophils reach the lungs and penetrate cancerous tissues, where they often release their destructive proteins and summon T-cells for reinforcement. Ultimately, T-cells gather in the affected lungs, slowing the growth of tumors. In the absence of eosinophils, lung metastases were much larger than those exposed to the white blood cells. These findings led to the conclusion that eosinophils could serve as a basis for improved immunotherapeutic medications to fight cancer effectively. “We chose to focus on lung metastases for two main reasons. First, metastases, and not the primary tumors, are often the main problem in treating cancer, and the lungs are a major target for the metastasis of many types of cancer,” said lead researcher Prof. Ariel Munitz of Tel Aviv University’s department of microbiology and clinical immunology. “Second, in a preliminary study we demonstrated that eosinophils gather in tumors developing in mucous tissues like the lungs, and therefore assumed that they would be found in lung metastases as well,” he added. Compared to traditional techniques like chemotherapy, immunotherapy generally leads to longer protection from cancer and fewer side effects. This new discovery may contribute to the development of new methods of immunotherapy. “Enhancing the number and power of T-cells is one of the main targets of immunotherapy treatments administered to cancer patients today,” said Munitz. To read the original article click here.

The post White Blood Cells May Be Harnessed to Boost Cancer Immunotherapy appeared first on Amazing Health Advances.

White Blood Cells Can Help Destroy Cancer Cells – Israeli Study

AHA Publisher — Thu, 16 Sep 2021 07:00:56 +0000

Jerusalem Post Staff via Jerusalem Post– A type of white blood cells known as eosinophils can help the body fight cancer, and are used to fight cancer metastasis (cancer cells breaking away from the original infection) in the lungs, a new study study from Tel Aviv University has revealed. Prof. Ariel Munitz and doctoral student Sharon Grisauri of the Department of Microbiology and Clinical IImmunology at the Sackler Faculty of Medicine led the research, which was published in the academic journal Cancer Research. Eosinophils are white blood cells in the immune system that produce destructive proteins, originally intended to fight parasites. The team examined biopsies of the lung metastases from breast cancer patients. They discovered that eosinophils reach the lungs and enter the cancer tissues, often releasing the destructive proteins they carry. High levels of hygiene, especially in the Western world, have significantly reduced parasites but eosinophils often react negatively to humans, as they introduce problems such as allergies and asthma. “We chose to focus on lung metastases of many types of cancer,” Munitz explained in a statement. “First, metastases, and not the primary tumors, are often the main problem in treating cancer, and the lungs are a major target for the metastasis of many types of cancer. Second, in a preliminary study, we demonstrated that eosinophils gather in tumors developing in mucous tissues like the lungs, and therefore assumed that they would be found in lung metastases as well.” For the testing, the researchers used animal models. The results showed that lung metastases developed in the absence of eosinophils that were much larger than those exposed to eosinophils. The conclusion was that eosinophils fight cancer effectively. But, how can eosinophils fight cancer effectively? “We observed that when eosinophils are missing, the tissue also lacks T-cells – white blood cells known for fighting cancer,” Munitz explained. “Consequently, we assumed that eosinophils combat cancer through T-cells. Our next task was to understand the mechanism underlying this process.” In essence, the eosinophils release chemokines, which summons T-cells, whenever they come into contact with cancer. This, essentially allows for the eosinophils to call for reinforcements, backing them up to better fight the cancer. These findings could help pave the way for improved cancer treatments in the future. To read the original article click here.

The post White Blood Cells Can Help Destroy Cancer Cells – Israeli Study appeared first on Amazing Health Advances.

Could a Fungus-Derived Compound Reduce Hyperinflammation in Severe COVID-19?

AHA Publisher — Wed, 23 Jun 2021 07:00:32 +0000

Angela Betsaida B. Laguipo, BSN via News-Medical – Drug repurposing for COVID-19 helps scientists identify potential drugs to treat COVID-19 without going through the rigorous process of formulation, clinical trials, and gaining regulatory body approval. Many of the drugs used for COVID-19 today were initially developed for other pathogens. Early-stage trials from scientists at the University of Pennsylvania, USA, demonstrates that cyclosporine A (CSA), a calcineurin inhibitor that modulates cytokine production, may have potential antiviral properties against coronaviruses. In the study, which appeared on the medRxiv* pre-print server, the researchers aimed to test whether a short course of CSA can help combat COVID-19. What Is Cyclosporine A (CSA)? Cyclosporine is a natural cyclic polypeptide immunosuppressant isolated from the fungus Beauveria nivea. Cyclosporine’s exact mechanism of action is unknown, but scientists believe it may involve binding to the cellular protein cytophilin, inhibiting the enzyme calcineurin. The complex CSA-cyclophilin interferes with a complex of phosphatases known as calcineurin that plays an imperative role in the immune response. The drug acts as an immunosuppressant commonly used after an organ transplant to reduce the immune system’s activity, preventing organ rejection. COVID-19 and Cytokine Storm The SARS-CoV-2 infection varies in severity, with a majority of patients experiencing mild to moderate illness. Severe pneumonia occurs in about 15 percent of cases and drives mortality. People who are at a higher risk of developing severe COVID-19 include the elderly, those who have compromised immune systems, and those with comorbidities. COVID-19 is characterized by immune dysregulation or a cytokine storm, an orchestrated response that involves infected cells, macrophages, T cells, and other immune cells. The cytokines or chemokines are produced and can affect the respiratory tract, causing widespread lung inflammation. Further, severe COVID-19 patients tend to have high interleukin 2 (IL-2), IL-7, IL-19, tumor necrosis factor (TNF), granulocyte colony-stimulating factor (G-CSF), C-X-C motif chemokine ligand 10 (CXCL10), monocyte chemoattractant protein 1 (MCP1), and macrophage inflammatory protein (MIP) in the blood. Increased levels of these cytokines, C-reactive protein (CRP), and ferritin, accompanied by lymphopenia, are usually seen in severely ill COVID-19 patients. These are hallmarks of patients experiencing macrophage activation syndrome. The Study The researchers tested whether a short course of treatment with CSA was safe for COVID-19 patients. They treated ten hospitalized but non-critically ill patients with CSA at an initial dose of 9mg/kg/day orally divided into dosing every 12 hours. The researchers conducted a therapeutic drug monitoring on the second day, and every Monday, Wednesday, and Friday during active dosing. The succeeding cyclosporine dosing was adjusted to target a trough level of 200 to 300ng/mL without a maximum dose level. During the treatment, five patients reported adverse effects, but none were serious. None of the enrolled participants needed intensive care unit-level care, and all patients were able to return home from the hospital. The researchers found that the CSA treatment was linked to reduced cytokine and chemokine levels in the blood, both of which are associated with hyper-inflammation in COVID-19. “In conclusion, short courses of CSA appear safe and feasible in COVID-19 patients requiring oxygen and therefore, may be a useful adjunct in resource-poor or resource-limited health care settings,” the team concluded in the study. One advantage of CSA is the cost-effectiveness of the treatment since drug acquisition costs are low, and it is widely available in oral pill and liquid formulations. Hence, the team showed that CSA is a potentially effective treatment for SARS-CoV-2 infection. It has anti-inflammatory properties, is widely available, low cost, and safe to use. With further research that corroborates the team’s findings, CSA may prove a cheap, safe and effective therapy for COVID-19 patients. *Important notice medRxiv publishes preliminary scientific reports that are not peer-reviewed and, therefore, should not be regarded as conclusive, guide clinical practice/health-related behavior, or treated as established information. This article has been modified. To read the original article click here.

The post Could a Fungus-Derived Compound Reduce Hyperinflammation in Severe COVID-19? appeared first on Amazing Health Advances.