Category Archives: Immunology

(Adds immunology expert's comment)

By Deena Beasley

Aug 28 (Reuters) - Researchers for the first time have identified someone in the United States who was reinfected with the novel coronavirus, according to a study that has not yet been reviewed by outside experts.

The report, published online, describes a 25-year-old man living in Reno, Nevada, who tested positive for the virus in April after showing mild illness. He got sick again in late May and developed more severe COVID-19, the disease caused by the virus.

"This study likely represents a clear example of reinfection ... reinfections are possible - which we already knew, because immunity is never 100%," Kristian Anderson, professor of immunology and microbiology at Scripps Research in La Jolla, California, said in an emailed comment.

Cases of presumed reinfection have cropped up in other parts of the world, but questions have arisen about testing accuracy. Earlier this week, University of Hong Kong researchers reported details of a 33-year-old man who had recovered in April from a severe case of COVID-19 and was diagnosed four months later with a different strain of the virus.

Researchers at the University of Nevada, Reno School of Medicine and the Nevada State Public Health Laboratory said they were able to show through sophisticated testing that the virus associated with each instance of the Reno man's infection represented genetically different strains.

They emphasized that reinfection with the virus is probably rare, but said the findings imply that initial exposure to the virus may not result in full immunity for everyone.

"We don't know at what frequency reinfections occur and how that might change over time," Anderson said. "Before we have broader studies illuminating these questions, we can't conclude what a single case of reinfection means for longevity and robustness of COVID-19 immunity and relevance for a future vaccine." (Reporting by Deena Beasley; Editing by Dan Grebler and Grant McCool)

Our Standards: The Thomson Reuters Trust Principles.

Immunology

Scientists Explore Why Some People Are Able To Live With An Infection Unscathed – KPCW

August 30, 2020 medical

One of the reasons Covid-19 has spread so swiftly around the globe is that for the first days after infection, people feel healthy. Instead of staying home in bed, they may be out and about, unknowingly passing the virus along. But in addition to these pre-symptomatic patients, the relentless silent spread of this pandemic is also facilitated by a more mysterious group of people: the so-called asymptomatics.

According to various estimates, between 20 and 45 percent of the people who get COVID-19 and possibly more, according to a recent study from the Centers for Disease Control and Prevention sail through a coronavirus infection without realizing they ever had it. No fever or chills. No loss of smell or taste. No breathing difficulties. They don't feel a thing.

Asymptomatic cases are not unique to COVID-19. They occur with the regular flu, and probably also featured in the 1918 pandemic, according to epidemiologist Neil Ferguson of Imperial College London. But scientists aren't sure why certain people weather COVID-19 unscathed. "That is a tremendous mystery at this point," says Donald Thea, an infectious disease expert at Boston University's School of Public Health.

The prevailing theory is that their immune systems fight off the virus so efficiently that they never get sick. But some scientists are confident that the immune system's aggressive response, the churning out of antibodies and other molecules to eliminate an infection, is only part of the story.

These experts are learning that the human body may not always wage an all-out war on viruses and other pathogens. It may also be capable of accommodating an infection, sometimes so seamlessly that no symptoms emerge. This phenomenon, known as disease tolerance, is well-known in plants but has only been documented in animals within the last 15 years.

Hints that 'disease tolerance' is at work

Disease tolerance is the ability of an individual, due to a genetic predisposition or some aspect of behavior or lifestyle, to thrive despite being infected with an amount of pathogen that sickens others. Tolerance takes different forms, depending on the infection. For example, when infected with cholera, which causes watery diarrhea that can quickly kill through dehydration, the body might mobilize mechanisms that maintain fluid and electrolyte balance. During other infections, the body might tweak metabolism or activate gut microbes whatever internal adjustment is needed to prevent or repair tissue damage or to make a germ less vicious.

"Why, if they have these abnormalities, are they healthy? Potentially because they have disease tolerance mechanisms engaged. These are the people we need to study." - Janelle Ayres, physiologist, Salk Institute for Biological Studies

Researchers who study these processes rely on invasive experiments that cannot be done in people. Nevertheless, they view asymptomatic infections as evidence that disease tolerance occurs in humans. At least 90 percent of those infected with the tuberculosis bacterium don't get sick. The same is true for many of the 1.5 billion of people globally who live with parasitic worms called helminths in their intestines. "Despite the fact that these worms are very large organisms and they basically migrate through your tissues and cause damage, many people are asymptomatic. They don't even know they're infected," says Irah King, a professor of immunology at McGill University. "And so then the question becomes, what does the body do to tolerate these types of invasive infections?"

While scientists have observed the physiological processes that minimize tissue damage during infections in animals for decades, it's only more recently that they've begun to think about them in terms of disease tolerance. For example, King and colleagues have identified specific immune cells in mice that increase the resilience of blood vessels during a helminth infection, leading to less intestinal bleeding, even when the same number of worms are present.

"This has been demonstrated in plants, bacteria, other mammalian species," King says.

"Why would we think that humans would not have developed these types of mechanisms to promote and maintain our health in the face of infection?" he adds.

Maybe germs aren't the enemy: A more nuanced view

In a recent Frontiers in Immunology editorial, King and his McGill colleague Maziar Divangahi describe their long-term hopes for the field: A deeper understanding of disease tolerance, they write, could lead to "a new golden age of infectious disease research and discovery."

Scientists have traditionally viewed germs as the enemy, an approach that has generated invaluable antibiotics and vaccines. But more recently, researchers have come to understand that the human body is colonized by trillions of microbes that are essential to optimal health, and that the relationship between humans and germs is more nuanced.

Meddlesome viruses and bacteria have been around since life began, so it makes sense that animals evolved ways to manage as well as fight them. Attacking a pathogen can be effective, but it can also backfire. For one thing, infectious agents find ways to evade the immune system. Moreover, the immune response itself, if unchecked, can turn lethal, applying its destructive force to the body's own organs.

"With things like COVID, I think it's going to be very parallel to TB, where you have this Goldilocks situation," says Andrew Olive, an immunologist at Michigan State University, "where you need that perfect amount of inflammation to control the virus and not damage the lungs."

Some of the key disease tolerance mechanisms scientists have identified aim to keep inflammation within that narrow window. For example, immune cells called alveolar macrophages in the lung suppress inflammation once the threat posed by the pathogen diminishes.

Much is still unknown about why there is such a wide range of responses to COVID-19, from asymptomatic to mildly sick to out of commission for weeks at home to full-on organ failure. "It's very, very early days here," says Andrew Read, an infectious disease expert at Pennsylvania State University who helped identify disease tolerance in animals. Read believes disease tolerance may at least partially explain why some infected people have mild symptoms or none at all. This may be because they're better at scavenging toxic byproducts, he says, "or replenishing their lung tissues at faster rates, those sorts of things."

Asymptomatic COVID-19 infections

The mainstream scientific view of asymptomatics is that their immune systems are especially well-tuned. This could explain why children and young adults make up the majority of people without symptoms because the immune system naturally deteriorates with age. It's also possible that the immune systems of asymptomatics have been primed by a previous infection with a milder coronavirus, like those that cause the common cold.

Asymptomatic cases don't get much attention from medical researchers, in part because these people don't go to the doctor and thus are tough to track down. But Janelle Ayres, a physiologist and infectious disease expert at the Salk Institute For Biological Studies who has been a leader in disease tolerance research, studies precisely the mice that don't get sick.

The staple of this research is something called the "lethal dose 50" test, which consists of giving a group of mice enough pathogen to kill half. By comparing the mice that live with those that die, she pinpoints the specific aspects of their physiology that enable them to survive the infection. She has performed this experiment scores of times using a variety of pathogens. The goal is to figure out how to activate health-sustaining responses in all animals.

A hallmark of these experiments and something that surprised her at first is that the half that survive the lethal dose are perky. They are completely unruffled by the same quantity of pathogen that kills their counterparts. "I thought going into this ... that all would get sick, that half would live and half would die, but that isn't what I found," Ayres says. "I found that half got sick and died, and the other half never got sick and lived."

Ayres sees something similar happening in the COVID-19 pandemic. Like her mice, asymptomatic people infected with the novel coronavirus seem to have similar amounts of the virus in their bodies as the people who fall ill, yet for some reason they stay healthy. Studies show that their lungs often display damage on CT scans, yet they are not struggling for breath (though it remains to be seen whether they will fully escape long-term impacts). Moreover, a small recent study suggests that people who are asymptomatic mount a weaker immune response than those who get sick suggesting that mechanisms are at work that have nothing to do with fighting infection.

"Why, if they have these abnormalities, are they healthy?" asks Ayres. "Potentially because they have disease tolerance mechanisms engaged. These are the people we need to study."

The goal of disease tolerance research is to decipher the mechanisms that keep infected people healthy and turn them into therapies that benefit everyone. "You want to have a drought-tolerant plant, for obvious reasons, so why wouldn't we want to have a virus-tolerant person?" Read asks.

A 2018 experiment in Ayres' lab offered proof of concept for that goal. The team gave a diarrhea-causing infection to mice in a lethal dose 50 trial, then compared tissue from the mice that died with those that survived, looking for differences. They discovered that the asymptomatic mice had utilized their iron stores to route extra glucose to the hungry bacteria, and that the pacified germs no longer posed a threat. The team subsequently turned this observation into a treatment. In further experiments, they administered iron supplements to the mice and all the animals survived, even when the pathogen dose was upped a thousandfold.

When the pandemic hit, Ayres was already studying mice with pneumonia and the signature malady of COVID-19, acute respiratory distress syndrome, which can be triggered by various infections. Her lab has identified markers that may inform candidate pathways to target for treatment. The next step is to compare people who progressed to severe stages of COVID-19 with those who are asymptomatic to see whether markers emerge that resemble the ones she's found in mice.

If a medicine is developed, it would work differently from anything that's currently on the market because it would be lung-specific, not disease-specific, and would ease respiratory distress regardless of which pathogen is responsible.

But intriguing as this prospect is, most experts caution that disease tolerance is a new field and tangible benefits are likely many years off. The work involves measuring not only symptoms but the levels of a pathogen in the body, which means killing an animal and searching all of its tissues. "You can't really do controlled biological experiments in humans," Olive says.

In addition, there are countless disease tolerance pathways. "Every time we figure one out, we find we have 10 more things we don't understand," King says. Things will differ with each disease, he adds, "so that becomes a bit overwhelming."

Nevertheless, a growing number of experts agree that disease tolerance research could have profound implications for treating infectious disease in the future. Microbiology and infectious disease research has "all been focused on the pathogen as an invader that has to be eliminated some way," says virologist Jeremy Luban of the University of Massachusetts Medical School. And as Ayres makes clear, he says, "what we really should be thinking about is how do we keep the person from getting sick."

Emily Laber-Warren directs the health and science reporting program at the Craig Newmark Graduate School of Journalism at CUNY.

This story was produced by Undark, a nonprofit, editorially independent digital magazine exploring the intersection of science and society.

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Scientists Explore Why Some People Are Able To Live With An Infection Unscathed - KPCW

Immunology

Blocking nerve signals to the pancreas halts type 1 diabetes onset in mice – Newswise

August 30, 2020 medical

Newswise LA JOLLAYour pancreas is a little sweet potato-shaped organ that sits snug behind your stomach. The pancreas is studded with islets, the cell clusters that house insulin-producing beta cells. In people with type 1 diabetes, the body's own immune cells head for the islets and start attacking the beta cells. No one knows exactly what triggers this attack.

One clue may lie in the pattern of beta cell death. Many beta cells are killed off in big patches while other beta cells are mysteriously untouched. Something seems to be drawing immune cells to attack specific groups of beta cells while ignoring others.

In a new Science Advances study, researchers at La Jolla Institute for Immunology (LJI) report that the nervous system may be driving this patchy cell die-off. Their new findings in a mouse model suggest that blocking nerve signals to the pancreas could stop patients from ever developing type 1 diabetes.

"It's astonishing that this process may be stoppable through neuronal influence," says LJI Professor Matthias von Herrath, M.D., who served as the studys senior author.

The von Herrath Lab has been working to uncover the cause of type 1 diabetes. Although there are environmental and genetic risk factors for the disease, type 1 diabetes often seemingly strikes at random. Over the years, researchers have sought an explanation for the observed patchy pattern of cell death. One theory has been that these patches have differences in blood flow or they have been damaged by a virus that might be sparking an immune attack.

But recently, researchers have been exploring a new field called neuroimmunology, which is the idea that nerve signals can affect immune cells. Could nerve signals drive immune cells to attack certain areas of the pancreas?

"We thought that could explain a lot," says study first author Gustaf Christoffersson, Ph.D., a former LJI postdoctoral researcher now at the University Uppsala, Sweden.

To test this theory, the researchers used a mouse model that can be experimentally induced to have beta cell death. They "denervated" the mice, either surgically or through use of a neurotoxin or a pharmacological agent, to block most of the sympathetic nerve signals to the pancreas. The researchers then used LJI's world-class imaging facility to track the pattern of beta cell death in living mice.

The team found that blocking the nerve signals protected mice from beta cell death, compared with no effect in mice given no treatment and mice given only beta blockers. Without innervation, it was like the pancreas had gone dark and immune cells were unable to find their target.

"We were pretty surprised to see that these nerve blockers led to pretty significant differences in the onset of diabetes," says Christoffersson.

More work needs to be done before this method can be tested in people. Von Herrath explains that doctors would first need a reliable way to identify patients at risk of type 1 diabetes onset. Once these patients are identified, von Herrath believes they could be treated either through electrostimulation or drugs to block nerve signals. There are also non-surgical, intravascular methods for blocking nerve signals.

The new discovery might explain much more than the patchiness seen in type 1 diabetes. Several autoimmune diseases share this same patchinessbut in a symmetrical pattern. For example, the skin condition vitiligo causes skin to lose its pigment, often in symmetrical areas across the faces and hands. Arthritis also tends to strike symmetrically, with inflammation in both knee, elbow or wrist joints.

The new study suggests that these areas may be innervated by nerves that branch out symmetrically through the body.

"This symmetry is very striking, and it's been almost impossible to explain," says von Herrath.

Von Herrath thinks breakthroughs in neuroimmunology could have broad implications for explaining why the body turns against its own organs in many autoimmune diseases. Going forward, he and Christoffersson hope to investigate the cellular mechanisms that connect the nervous system and type 1 diabetes.

The study, "Interference with pancreatic sympathetic signaling halts the onset of diabetes in mice," was supported by the National Institutes of Health (R01 AI092453), the Swedish Research Council (2014-06840 and 2018-02314), the Swedish Society for Medical Research, the Gran Gustafsson Foundation, and the Science for Life Laboratory.

The study was co-authored by Sowbarnika S. Ratliff of LJI.

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About La Jolla Institute for Immunology

The La Jolla Institute for Immunology is dedicated to understanding the intricacies and power of the immune system so that we may apply that knowledge to promote human health and prevent a wide range of diseases. Since its founding in 1988 as an independent, nonprofit research organization, the Institute has made numerous advances leading toward its goal: life without disease.

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Blocking nerve signals to the pancreas halts type 1 diabetes onset in mice - Newswise

Immunology

Interrogating the Immunology of Infectious Disease with Single-Cell and Spatial Multiomics – Genetic Engineering & Biotechnology News

August 22, 2020 medical

Broadcast Date: September 22, 2020Time: 8:00 am PT, 11:00 am ET, 17:00 CET

The incredible speed with which the current coronavirus has infected and spread to millions of people across the globe underscores the importance of better understanding the immune response to infectious diseases. The human immune system orchestrates sophisticated and coordinated reactions to foreign pathogens, but appreciating how individual immune cells respond to each challenge is key to uncovering the hidden parts of immunity.

In thisGENwebinar, we will discuss the utility of single-cell and spatial multiomics technologies to advance infectious disease and immunology research, highlighting how the scientific community can respond to such events as the COVID-19 pandemic. Our webinar panelist, Dr. Brian Fritz, will take us through a comprehensive assessment of the adaptive immune repertoire and phenotypic immune responses to infectious disease using single-cell sequencing technologies. Additionally, he will tell us how infectious disease researchers can integrate single cell and spatial multiomic technology from 10x Genomics to identify cell states in a sample and map their location within intact tissue. Finally, you will learn about mapping adaptive immunity to antigen specificity and accelerating novel neutralizing antibody discovery with multiomic readouts at single-cell resolution.

A live Q&A session will follow the presentation, offering you a chance to pose questions to our expert panelists.

Produced with support from:

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Interrogating the Immunology of Infectious Disease with Single-Cell and Spatial Multiomics - Genetic Engineering & Biotechnology News

Immunology

Cancer Immunology And Oncolytic Virology Market Insights on Scope the COVID-19 – Scientect

August 22, 2020 medical

The global cancer immunotherapy market should reach $96.5 billion by 2021 from $73.0 billion in 2016 at a compound annual growth rate (CAGR) of 5.7%, from 2016 to 2021.

Report Scope:

The scope of this report covers current cancer immunotherapy markets for most common cancers. The market segments included in this report are therapeutic monoclonal antibodies (with special focus on checkpoint inhibitors), synthetic interleukins, interferons, and colony-stimulating factors; small kinase inhibitors of cancer-related targets; protective and therapeutic cancer vaccines; and adoptive cell therapies. This report also covers treatments that are in development for late-stage and early-stage oncolytic viruses. Detailed epidemiological information, discussion of incidence and mortality trends, overview of regulatory landscapes, and analysis of market shares for leading products and companies are also included in this report.

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Report Includes:

An overview of the global markets for cancer immunotherapies and oncolytic virology. Analyses of global market trends, with data from 2015, 2016, and projections of compound annual growth rates (CAGRs) through 2021. Analyses of factors influencing market demand, such as clinical guidelines, demographic changes, and market saturation. Information covering the latest trends, market structure, market size, key drug segments, and trends in technology. Coverage of colony stimulating factors (CSFs), interferon alfa and gamma products, interleukin products and therapeutic monoclonal antibodies, including antibody conjugates, cancer vaccines, and other cancer treatment immunology products. Technological discussions, including the current state, newly issued patents, and pending applications. Profiles of leading companies in the industry.

Report Summary

Cancer is a disease with global implications. There are many different types of cancer, of which the most common types include lung, breast, colon and rectal, stomach, head and neck, prostate, cervical, melanoma, and ovarian cancer, as well as leukemia. Cancer is a genetic disease that is conventionally treated by surgery, radiation therapy, chemotherapy, hormonal therapy, and immunotherapy. Surgery is the mainstay treatment for all cancers. Usually surgery is complimented with radiation or chemotherapy to ensure the clearance of all residual cancer. Despite the advances in treatment, cancer has great plasticity; therefore, after a certain time the effects of treatment fade and cancer returns with acquired resistance. Combination therapy, using multiple modalities including surgery and pharmaceutical or radiation therapy, improves response to treatment.

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Radiation and chemotherapy have many side effects. Biological treatment options provide less impactful treatment of cancer. Immunotherapy is a type of biological therapy and it incorporates elements of the immune system in cancer treatment. The immune system has various types of cells and proteins that detect and act upon signs of a disease or infection by harmful and foreign substances such as microbes, bacteria and viruses. The immune system differentiates the bodys own cells and tissues through an evolutionary bar-coding system. This system helps the immune system understand encountered foreign substances as nonself. Cancer cells are recognized as nonself as well. The immune system monitors the body for cancer and destroys when it detects a malignancy. Cancer cells can avoid being recognized by the immune system and develop resistance through numerous methods.

Since the early 1900s, the connection between cancer and the immune system has caught the attention of various scientists and medical practitioners. Although the early studies were bluntly done without current technological and scientific tools, they nonetheless shed insights leading to the development of the first monoclonal antibodies and to the use of biologically derived synthetic interleukins and interferons. After many decades of research, immunotherapy finally emerged as a fully functionalclinical area in the 1990s. Since then, the cancer therapeutics landscape has changed dramatically.

With the stream of product approvals in recent years, the global immunotherapy market has reached its current value. In 2015, the global cancer immunotherapy market hit $65 billion. The current immunotherapy market contains several blockbuster products reaching their end-of-market exclusivities; however, the market is mostly comprised of newly introduced and expensive therapies. In 2016, the market expanded by more than 10% over the previous year, reaching $73 billion. During the period of 2016 through 2021, the global cancer immunotherapy market is forecast to grow by a 5.7% compound annual growth rate (CAGR), reaching $96.5 billion in 2021.

The strongest growth is expected to occur in checkpoint-inhibitor drugs with a 19.4% CAGR during the forecast period. Immunomodulators are anticipated to show the second-highest growth rates among immunotherapy products, with an 8.4% CAGR during the same period. The combined sales from both segments are expected to make up for nearly one-third of the market, with a combined sales value of $28 billion in 2021. Checkpoint inhibitors are virtually comprised of monoclonal antibodies; however,they are assessed separately due to their immense commercial and clinical significance. Sales from other therapeutic antibodies accrued to $28 billion in 2016, and this value is expected to remain relatively constant through 2021, due to several patent expiries, pressure from anticipated generic entries, and newly introduced classes of drugs expected by 2021.

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Cancer Immunology And Oncolytic Virology Market Insights on Scope the COVID-19 - Scientect

Immunology

Some have no COVID symptoms: Could the common cold be a reason? – ABC News

August 22, 2020 medical

August 22, 2020, 5:19 PM

5 min read

Some infected with the novel coronavirus never develop symptoms. Others get very sick and die. Seven months into the pandemic, scientists are racing to find out why.

There are theories. One theory is that prior exposure to other viruses may help fight off the novel coronavirus. There are four other, far less deadly coronaviruses which cause the common cold.

Earlier this summer, researchers from La Jolla Institute for Immunology published new findings in the journal Cell, offering insight into how human immune systems respond to COVID-19. When people who were previously infected with COVID-19 were exposed to the virus again, their immune system had a strong response because it already knew what the virus looked like.

But what researchers also found was that in around 40 to 60% of those who had never been exposed to COVID-19, their immune systems also had a strong reaction. The researchers said it's possible that human bodies may "recognize" the novel coronavirus because of prior exposure to its close cousins -- the coronavirus strains that cause the common cold.

"Immune reactivity may translate to different degrees of protection," said Dr. Alessandro Sette, professor at the La Jolla Institute for Immunology and a lead author on the study, in a press release.

It's possible, Sette said, that your prior infections with the common cold could give your immune system a boost, making it easier to fight off the coronavirus that causes COVID-19.

Many viruses fall under the coronavirus category, including ones that cause the common cold, SARS and MERS.

A study in Science published early August looked at blood samples obtained before the COVID-19 pandemic was discovered. Isolating immune system cells from those samples, scientists found that those cells reacted similarly to the COVID-19 virus as well as to four other coronaviruses known to cause the common cold.

"This could help explain why some people show milder symptoms of disease while others get severely sick," said Dr. Daniela Weiskopf, a research assistant professor at the La Jolla Institute for Immunology and one of the lead researchers, in a statement.

And while almost everyone has had a cold at least once in their life, COVID-19 still affects some people more severely than others. That reason may have more to do with genetics, than previous exposure to the common cold, some experts say.

"People have this idea that we are all pretty much the same. But there is huge variation in our genes in the human population," said Dr. Vincent Racaniello, Higgins professor of Microbiology and Immunology at Columbia University. "Everyone is genetically different. You can find kids who get respiratory infections 10 to 12 times a year, totally atypical. And when you look at their genome, you find that they have mutations that make them more susceptible."

Meanwhile, some scientists say the differences in the way people fare once infected could be chalked up to ailing immune systems among the elderly.

"What we know is that as you age your immune system degrades. It's called 'immunosenescence.' You are not able to control infections like you were used to. So the infection goes a little bit crazy at the beginning. You overreact and you get very sick," said Racaniello.

In the meantime, researchers continue to look at the immune system for answers to fighting COVID-19.

Jonathan Chan, M.D., is an emergency medicine resident at St. John's Riverside Hospital and a contributor to the ABC News Medical Unit.

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Some have no COVID symptoms: Could the common cold be a reason? - ABC News

Immunology

Immunology Drug Market Forecasted To Surpass The Value Of US$ XX Mn/Bn By 2017 2025 – Scientect

August 22, 2020 medical

Given the debilitating impact of COVID-19 (Coronavirus) on the Immunology Drug market, companies are vying opportunities to stay afloat in the market landscape. Gain access to our latest research analysis on COVID-19 associated with the Immunology Drug market and understand how market players are adopting new strategies to mitigate the impact of the pandemic.

Analysis of the Global Immunology Drug Market

Persistence Market Research (PMR) recently published a market study which provides a detailed understanding of the various factors that are likely to influence the Immunology Drug market in the forecast period (20XX-20XX). The study demonstrates the historical and current market trends to predict the roadmap of the Immunology Drug market in the coming years. Further, the growth opportunities, capacity additions, and major limitations faced by market players in the Immunology Drug market are discussed.

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Regional Overview

Our team of analysts at PMR, trace the major developments within the Immunology Drug landscape in various geographies. The market share and value of each region are discussed in the report along with graphs, tables, and figures.

Competitive Outlook

This chapter of the report discusses the ongoing developments, mergers and acquisitions of leading companies operating in the Immunology Drug market. The product portfolio, pricing strategy, the regional and global presence of each company is thoroughly discussed in the report.

Product Adoption Analysis

The report offers crucial insights related to the adoption pattern, supply-demand ratio, and pricing structure of each product.

key players and products offered

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Immunology

Key molecule can be used to assess prognosis of triple negative breast cancer – News-Medical.Net

August 22, 2020 medical

Hokkaido University scientists have shown that Interleukin-34 is a prognostic marker and drug target for Triple Negative Breast Cancer.

Breast cancer is the most common cancer among women across the world, affecting 28.9% . Depending on the combination of cell receptor molecules present on the surface of the cancer cells, breast cancer is classified into one of three types: Luminal A, Luminal B and HER2+.

The receptors determine which hormone the cancer is dependent on for survival, and thus indicate which drugs can be used to treat the cancer. A fourth type of breast cancer, Triple Negative Breast Cancer (TNBC), does not have any of these three receptors. This type of cancer does not respond to standard treatments and the prognosis is generally poorer than for other types of breast cancer.

A team of scientists from the Institute for Genetic Medicine (IGM) at Hokkaido University have established a link between a molecule called interleukin-34 (IL-34) and Triple Negative Breast Cancer, and have shown that IL-34 can be used to assess prognosis of TNBC patients. Their findings were published in the specialist journal Breast Cancer.

Interleukin-34 (IL-34) is a cytokine, a type of molecule that transmits signals between cells and is responsible for fighting disease. IL-34 is known to associate well with poor outcomes in lung cancer and liver cancer, among others. For this reason, the scientists decided to determine the relationship between IL-34 and TNBC.

Data from 1083 breast cancer patients was obtained from The Human Cancer Genome Atlas (TCGA) and was statistically analyzed. The scientists investigated the correlation between IL-34 and each type of cancer. They discovered that TNBC is associated with high levels of IL-34. When they looked into the effect of IL-34 on prognosis, they found that the prognosis for TNBC patients with high IL-34 levels was poor.

To demonstrate that this relationship could be replicated in the lab, experiments were carried out in mice models. The scientists compared the growth and development of two cell lines that were identical except for the levels of IL-34 expressed: one cell line expressed high levels of IL-34 while the other expressed low levels.

In cell culture, there was no difference observed between the cell lines; however, once introduced into mice, the cells that expressed high levels of IL-34 caused rapid tumor growth. They discovered that IL-34 promotes creation of a favourable environment for the growth of tumors by protecting them from anti-tumor macrophages.

The group that conducted this study was led by Professor Ken-ichiro Seino, head of the Division of Immunology, IGM.

Currently, chemotherapy is the only reliable means of treating TNBC, but it frequently develops resistance to chemotherapy. Our findings show that IL-34 is an attractive molecular target for targeted cancer therapy."

Ken-ichiro Seino, Professor and Head of Division of Immunology, Institute for Genetic Medicine

For the last five years, Seino's lab has worked on the relationship between IL-34 and different types of cancer. In a closely related study, his group has shown that treatments to reduce IL-34 leads to reduced tumor growth in mice; what remains to be studied is whether this can be used in humans, and how effective it will be.

Source:

Journal reference:

Kajihara, N., et al. (2020) Interleukin-34 contributes to poor prognosis in triple-negative breast cancer. Breast Cancer. doi.org/10.1007/s12282-020-01123-x.

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Key molecule can be used to assess prognosis of triple negative breast cancer - News-Medical.Net

Immunology

Immunology Professor Paul Moynagh says hes perplexed by Government decision putting sport behind closed doo – The Irish Sun

August 19, 2020 medical

IMMUNOLOGY Professor Paul Moynagh says he's 'perplexed' by the Government's decision to put sport behind closed doors.

He cannot understand why it's being limited so much when it's been established that outdoor activity is far less risky than indoors.

He told RTE: "I'm probably perplexed actually with some of the decisions.

"I like to see decisions based on an evidence base and it seems like putting sport behind closed doors again and 200 spectators not being able to attend, that doesn't make sense to me.

"We know how this virus is transmitted.

"The risk of it being transmitted outdoors is significantly less than inside."

Taoiseach Micheal Martin this evening announced that all sport would go behind closed doors until September 13 at the earliest.

Acting CMO Ronan Glynn identified the gathering of people before and after matches as being the primary concern rather than during the matches themselves.

Researchers Get First-Ever Look at a Rare but Vital Stem Cell in Humans – Technology Networks

August 19, 2020 medical

Neutrophils are the warriors of the immune system. They are always ready to spring to action to help heal injuries or fight off disease. Unless, that is, something goes wrong in their developmental process.Immature neutrophils arent all warriors they can be dangerous turncoats. High levels of immature neutrophils in the bloodstream can be a tell-tale sign of cancer and may even be a biomarker for COVID-19.

Now scientists at La Jolla Institute for Immunology (LJI) have tracked down the rare stem cells that generate neutrophils in human bone marrow. This research, published in Immunity, gives researchers a potential path for intervening in diseases where neutrophil development goes awry.

We have identified the stem cells that are the early origins of neutrophils, the most abundant blood cell type in humans, says Huy Dinh, Ph.D., a former LJI postdoctoral associate who recently moved to a faculty position at The University of WisconsinMadison. Dinh led the study with LJI Professor Catherine C. Hedrick, Ph.D. Knowing how human neutrophils develop is especially relevant today because immature neutrophils have been found to be elevated in both the blood and lungs of severe COVID-19 patients.

Despite their importance, neutrophils have proven very hard to study. They dont hold up well outside the body, and the stem cells that make them are even harder to investigate because they only live in bone marrow.

In 2018, the Hedrick Lab reported the discovery of a group of progenitor stem cells that give rise to mature neutrophils. These progenitors sole job was to generate neutrophils, yet they appeared to also promote tumor growth. The researchers believed that detecting these progenitors could give doctors a better way to catch early cancer cases. But first, the team needed to know a lot more about neutrophil development.

The new research revealed a progenitor cell type that exists even earlier in human neutrophil development. Dinh, a past SPARK Award recipient, together with Tobias Eggert, Ph.D., a LJI visiting scientist and Melissa Meyer, Ph.D., a LJI postdoc, who served as the co-first authors in the study, spearheaded the effort to use a tool called cytometry by time-of-flight (CyTOF) to distinguish these rare cells from other types of immune progenitor cells. This work also made it possible for the researchers to identify more specific protein markers on this early progenitor cell surface.

The discovery of these protein markers was important because until now, scientists have used only a few of markers to track neutrophils over time. The new study gives scientists specific markers for tracking neutrophil development from day one.

The researchers also found that cases of skin and lung cancers are often accompanied by a flood of immature neutrophils including the early progenitor cells into the bloodstream. These immature neutrophils change as they interact with tumor cells, though the researchers arent sure yet how these changes affect cancer progression.

Dinh likens the stages of neutrophil development to the cars on a train. The early progenitors are like the train engine, keeping everything going smoothly along the track to maturity. Cancer shakes everything up, and immature neutrophils jump off the track before they reach maturity. Its like the train is falling apart, Dinh says.

Neutrophil development has been in the news recently due to the COVID-19 pandemic, as studies have shown immature neutrophils are also more abundant in some patients with COVID-19. Dinh and Hedrick think perhaps the threat of the virus prompts the body to churn out neutrophils too quickly, again forcing immature cells off the track to maturity.

We need to study this phenomenon further to see if these neutrophils can be tied to case prognosis or if they can be a drug target for COVID-19, says Dinh.

The researchers hope to continue their work to discover the exact mechanisms that stop neutrophils from reaching maturity. Knowing the earliest cell that gives rise to neutrophils is really critical for trying to target and control these cells, says Hedrick. But we dont know exactly how to do that yet.

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Researchers Get First-Ever Look at a Rare but Vital Stem Cell in Humans - Technology Networks