New Method Uncovers How Viruses Evade Immune Responses — and How We Might Fight Back

Co-first authors Erin Doherty (left) and Jason Nomburg (right)
Photo Credit: Courtesy of Innovative Genomics Institute

Viruses and their hosts — whether bacteria, animals, or humans — are locked in a constant evolutionary arms race. Cells evolve defenses against viral infection, viruses evolve ways around those defenses, and the cycle continues.

One important weapon that cells use in the fight against viruses is a set of tiny molecular “alarm signals” made of nucleotides: the same chemical building blocks that make up DNA and RNA. When a virus infects a cell, these nucleotide messengers activate powerful immune defenses. To survive, viruses must find ways to shut these signals down. In a new study published in the journal Cell Host & Microbe, IGI researchers reveal that viruses have evolved a surprisingly large and diverse set of enzymes specifically designed to destroy these immune alarm signals, helping them hide from or disable the host’s antiviral defenses.

Immune cells turn damage into repair

Intestines one week after abdominal irradiation, showing proliferating epithelial cells (in brown).
Image Credit: Julius Fischer / TUM 

Patients receiving intensive cancer treatments often suffer from severe damage to the intestinal lining. Researchers from the Technical University of Munich (TUM) and the Leibniz Institute for Immunotherapy (LIT) have discovered that certain immune cells can trigger healing processes. They use inflammatory signals to do so - which is surprising, as inflammation in the intestine was previously thought to be primarily harmful. This finding could open new possibilities for therapies. 

Regulatory T cells (Tregs), a specialized type of immune cells, are usually seen as “peacekeepers” that prevent excessive immune attacks. In a study  published in Signal Transduction and Targeted Therapy, researchers from the Department of Radiation Oncology at the TUM University Hospital and the LIT Cooperation Group “Innate Immune Sensing in Cancer and Transplantation” uncovered how the body's own immune system can be harnessed to repair the intestinal lining and improve survival.  

Immunology: In-Depth Description

Image Credit: Scientific Frontline / AI generated

Immunology is the branch of biomedical science concerned with the structure, function, and disorders of the immune system—the complex network of cells, tissues, and organs that protect an organism from foreign invaders. Its primary goal is to understand how biological systems identify and eliminate pathogens (such as bacteria, viruses, fungi, and parasites) while maintaining tolerance for the body's own healthy tissue (distinguishing "self" from "non-self").

Why the "gut brain" plays a central role for allergies

This tissue section, taken from the intestine of a mouse unable to produce the neuropeptide VIP, clearly shows the striking frequency with which certain cell types occur on the intestine's surface. These include villous cells (red), mucus-producing goblet cells (yellow), Paneth cells (pink) and stem cells (green).
Image Credit: © Charité | Luisa Barleben

The intestinal nervous system, often referred to as the "gut brain", is essential in controlling digestion and maintaining the intestinal barrier. This protective layer, made up of the intestinal mucosa, immune cells and the microbiome, shields the body from the contents of the gut. Its effectiveness depends on the delicate balance among these components. If this balance is disrupted, inflammation, allergies, or chronic intestinal diseases can arise. The intestinal mucosa serves as the body’s primary defense against pathogens. While previous studies have shown that the intestinal nervous system is involved in immune responses in addition to digestion, its role in the development of intestinal epithelial cells has remained largely unclear until now. 

LJI scientists discover how T cells transform to defend our organs

The new study was led by Pandurangan Vijayanand, M.D., Ph.D., William K. Bowes Distinguished Professor at La Jolla Institute for Immunology
Photo Credit: Courtesy of La Jolla Institute for Immunology

We owe a lot to tissue resident memory T cells (TRM). These specialized immune cells are among the body’s first responders to disease. 

Rather than coursing through the bloodstream—as many T cells do—our TRM cells specialize in defending specific organs. They battle viruses, breast cancer, liver cancer, melanomas, and many other health threats. 

Pandurangan Vijayanand, M.D., Ph.D., William K. Bowes Distinguished Professor at La Jolla Institute for Immunology (LJI), has even shown that a greater density of TRM cells is linked to better survival outcomes in lung cancer patients.

Customised cells to fight brain cancer

Visualisation of cell death induced by CAR-T cells. A real-time imaging experiment (images taken at 0, 5 and 10 minutes) shows a CAR-T cell in contact with a glioblastoma cell (artificially marked in green). This contact causes the CAR-T cell to concentrate granules (lytic granules, shown in pink) containing the proteins necessary for the death of the target cell. These proteins penetrate the cancer cell and induce its death. After 10 minutes, the cancer cell begins to die, as indicated by the loss of its structure (evidenced by the appearance of "bubbles").
Image Credit: © Denis Migliorini

With a five-year survival rate of less than 5%, glioblastoma is one of the most aggressive types of brain cancer. Until now, all available treatments, including immunotherapy — which involves strengthening the immune system to fight cancer— have proved disappointing. CAR-T cells are genetically modified immune cells manufactured in the laboratory and designed to identify and destroy cancer cells. By targeting a protein present in the tumor environment, a team from the University of Geneva (UNIGE) and the Geneva University Hospital (HUG) has developed CAR-T cells capable of destroying glioblastoma cells. Their efficacy in an animal model of the disease paves the way for clinical trials in humans. These results are published in the Journal for ImmunoTherapy of Cancer. 

A cellular protein, FGD3, boosts breast cancer chemotherapy, immunotherapy

The research team included, front row, from left: graduate student Junyao Zhu, biochemistry professor David Shapiro, and senior researcher Chengiian Mao; back row, from left: graduate students Abigail Spaulding, Xinyi Dai and Qianjin Jiang.
Photo Credit: Fred Zwicky

A naturally occurring protein that tends to be expressed at higher levels in breast cancer cells boosts the effectiveness of some anticancer agents, including doxorubicin, one of the most widely used chemotherapies, and a preclinical drug known as ErSO, researchers report. The protein, FGD3, contributes to the rupture of cancer cells disrupted by these drugs, boosting their effectiveness and enhancing anticancer immunotherapies.

The new findings were the happy result of experiments involving ErSO, an experimental drug that killed 95-100% of estrogen-receptor-positive breast cancer cells in a mouse model of the disease. ErSO upregulates a cellular pathway that normally protects cancer cells from stress, said University of Illinois Urbana-Champaign biochemistry professor David Shapiro, who led the new work with Illinois graduate student Junyao Zhu. But when that protective pathway is ramped up, the system goes awry.

Combination of immunotherapy and targeted therapy improves survival for patients with advanced colorectal cancer

Human colorectal cancer cells
Image Credit: National Cancer Institute

A new study led by UCLA investigators found that combining zanzalintinib, a targeted therapy drug, and atezolizumab, an immune checkpoint inhibitor, helped patients with metastatic colorectal cancer, the second most common cause of cancer death in the U.S., live longer and control their disease better than with the standard treatment drug regorafenib. 

The findings simultaneously published in The Lancet and presented at the European Society for Medical Oncology Congress; mark the first time an immunotherapy-based regimen has demonstrated a survival benefit in the vast majority of patients with metastatic colorectal cancer.

“This study represents an important step forward for a group of patients who have historically had very few treatment options,” said Dr. J. Randolph Hecht, professor of clinical medicine at the David Geffen School of Medicine at UCLA and first author of the study. “We may finally be finding ways to make immunotherapy work for more patients with colorectal cancer.”

Why women's brains face higher risk: scientists pinpoint X-chromosome gene behind MS and Alzheimer's

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New research by UCLA Health has identified a sex-chromosome linked gene that drives inflammation in the female brain, offering insight into why women are disproportionately affected by conditions such as Alzheimer’s disease and multiple sclerosis as well as offering a potential target for intervention. 

The study published in the journal Science Translational Medicine, used a mouse model of multiple sclerosis to identify a gene on the X chromosome that drives inflammation in brain immune cells, known as microglia. Because females have two X chromosomes, as opposed to only one in males, they get a “double dose” of inflammation, which plays a major role in aging, Alzheimer’s disease and multiple sclerosis.  

When the gene, known as Kdm6a, and its associated protein were deactivated, the multiple sclerosis-like disease and neuropathology were both ameliorated with high significance in female mice.  

Checkpoint Inhibitor Promotes Tissue Repair

The illustration shows the mechanism of action of immune checkpoint inhibitors: antibodies (yellow) activate T cells (blue) enabling them to recognize and attack tumor cells (purple) more effectively. At the same time, checkpoint inhibitors accelerate tissue healing.
Image Credit: Scientific Frontline / AI generated

The body employs a protective mechanism that curbs overzealous immune responses. Known as checkpoint inhibitors, this natural braking system is located on the surface of certain immune cells. Cancer therapy often disables these inhibitors so that the immune system can fight tumor cells more effectively.

Previous observations showed that one of these inhibitors, known as TIGIT, provides a certain level of protection against tissue damage in mice infected with viruses. “We suspected that TIGIT also has something to do with tissue repair. However, the underlying mechanisms were completely unknown until now,” says Nicole Joller, Professor of Immunology at the Department of Quantitative Biomedicine at the University of Zurich (UZH). Joller’s team recently identified the signaling pathway that TIGIT uses to promote tissue repair.

A promising target for multiple sclerosis

The image depicts a neuron with its axon insulated by segments of the myelin sheath. The visible degradation and fragmentation of that sheath represent the demyelination process that is characteristic of multiple sclerosis. This process disrupts the neuron's ability to transmit signals efficiently, leading to the neurological symptoms associated with the condition.
Image Credit: Scientific Frontline / AI generated

A team from UNIGE and HUG has discovered a subgroup of immune cells particularly involved in the disease, paving the way for more precise treatments and avoiding certain side effects.

Multiple sclerosis, which affects around one in 500 people in Switzerland, is an autoimmune disease in which immune cells attack the central nervous system, causing irreversible damage. Current treatments involve blocking the immune system to prevent it from attacking the body. Although effective, these drugs can trigger potentially serious infections. A team from the University of Geneva (UNIGE) and Geneva University Hospitals (HUG), in collaboration with the University of Pennsylvania, has identified a subtype of immune cells in newly diagnosed patients that may have a decisive role in disease progression.  A treatment targeting these cells specifically could effectively control the disease while avoiding certain side effects. These findings have been published in the journal Annals of Neurology.

AI tool offers deep insight into the immune system

scHDeepInsight.
An overview of the process linking single-cell RNA input, image conversion and CNN analysis, to hierarchical immune cell classification.
Image Credit: ©2025 Tsunoda et al.
(CC BY-ND 4.0)

Researchers explore the human immune system by looking at the active components, namely the various genes and cells involved. But there is a broad range of these, and observations necessarily produce vast amounts of data. For the first time, researchers including those from the University of Tokyo built a software tool which leverages artificial intelligence to not only offer a more consistent analysis of these cells at speed but also categorizes them and aims to spot novel patterns people have not yet seen.

Our immune system is important — it’s impossible to imagine complex life existing without it. This system, comprising different kinds of cells, each playing a different role, helps to identify things that threaten our health, and take actions to defend us. They are both very effective, but also far from perfect; hence, the existence of diseases such as the notorious acquired immunodeficiency syndrome, or AIDS. And recent earth-shattering issues, such as the coronavirus pandemic, serve to highlight the importance of research around this intricate yet powerful system.

Engineered “natural killer” cells could help fight cancer

Caption:A new study identifies genetic modifications that make “natural killer” cells more effective at destroying cancer cells.
Image Credit: NIAID
(CC BY-NC-ND 4.0)

One of the newest weapons that scientists have developed against cancer is a type of engineered immune cell known as CAR-NK (natural killer) cells. Similar to CAR-T cells, these cells can be programmed to attack cancer cells.

MIT and Harvard Medical School researchers have now come up with a new way to engineer CAR-NK cells that makes them much less likely to be rejected by the patient’s immune system, which is a common drawback of this type of treatment.

The new advance may also make it easier to develop “off-the-shelf” CAR-NK cells that could be given to patients as soon as they are diagnosed. Traditional approaches to engineering CAR-NK or CAR-T cells usually take several weeks.

“This enables us to do one-step engineering of CAR-NK cells that can avoid rejection by host T cells and other immune cells. And, they kill cancer cells better and they’re safer,” says Jianzhu Chen, an MIT professor of biology, a member of the Koch Institute for Integrative Cancer Research,and one of the senior authors of the study.

Antibody discovered that blocks almost all known HIV variants in neutralization assays

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 A Cologne-led research team has discovered the antibody 04_A06, which neutralizes the human immunodeficiency virus (HIV) in almost all tested variants in vitro and even overcomes typical resistance mechanisms. The discovery potentially opens up new perspectives for the prevention and treatment of HIV infections.

An international research team led by the University of Cologne has discovered an antibody that could advance the fight against HIV. The newly identified antibody 04_A06 proved to be particularly effective in laboratory tests. It was able to neutralize 98.5 percent of more than 300 different HIV strains, making it one of the broadest antibodies against HIV identified. In experiments with humanized mice – animals whose immune system has been modified to resemble that of humans – 04_A06 permanently reduced the HIV viral load to undetectable levels. Most other HIV antibodies, in contrast, only achieve short-term effects in this animal model, as resistance develops quickly. The study ‘Profiling of HIV-1 elite neutralizer cohort reveals a CD4bs bNAb for HIV-1 prevention and therapy’ was published in Nature Immunology.

New mechanism revealed: How leukemia cells trick the immune system

Thoas Fioretos, Niklas Landberg, and Carl Sandén are the research team behind the study now being published in Nature Cancer.
Photo Credit: Tove Smeds

A research team at Lund University in Sweden has discovered a mechanism that helps acute myeloid leukemia cells to evade the body’s immune system. By developing an antibody that blocks the mechanism, the researchers could restore the immune system’s ability to kill the cancer cells in laboratory trials and in mice. The discovery is published in Nature Cancer.

Immunotherapy has improved the treatment for many cancers, but progress has been limited in leukemia. Acute myeloid leukemia (AML) is particularly intractable, with a five-year survival rate of just over 30 per cent. The existing treatments are often aggressive and may include both strong chemotherapy and stem cell transplantations.

“We wanted to see if we could find surface proteins unique to leukemia stem cells, and which would therefore act as interesting targets for a targeted treatment. If such proteins were not present on healthy blood stem cells it might be possible to attack the tumor – without harming the healthy blood system,” says Thoas Fioretos, research group leader and professor of clinical genetics at Lund University, and senior consultant at Skåne University Hospital.