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Comment by Dr. Krishna Kumari Challa on August 17, 2025 at 9:41am

Aging Can Spread Through Your Body Via a Single Protein

ReHMGB1. A new study pinpoints this protein as being able to spread the wear and tear that comes with time as it quietly travels through the bloodstream. This adds significantly to our understanding of aging.

Short for reduced high mobility group box 1, ReHMGB1 triggers senescence in cells, permanently disabling them. It doesn't just do this locally; it can send damaging signals throughout the body, particularly in response to injuries or disease.

This study reveals that aging signals are not confined to individual cells but can be systemically transmitted via the blood, with ReHMGB1 acting as a key driver

The findings could help develop ways to keep us healthier for longer. If we can block or control this protein's signals, it might slow the cascade of cellular decline that comes with age.

The researchers were able to identify ReHMGB1 as a critical messenger passing on the senescence signal by analyzing different types of human cells grown in the lab and conducting a variety of tests on mice.

When ReHMGB1 transmission was blocked in mice with muscle injuries, muscle regeneration happened more quickly, while the animals showed improved physical performance, fewer signs of cellular aging, and reduced systemic inflammation.

By blocking this pathway, scientists were able to restore tissue regenerative capacity, suggesting a promising strategy to treat aging-related diseases.

This process is only one contributor to aging out of many, but the signals that ReHMGB1 spreads are particularly important in terms of our bodies becoming dysfunctional over time and less able to carry out repairs.

https://www.metabolismjournal.com/article/S0026-0495(25)00128-3/fulltext

Comment by Dr. Krishna Kumari Challa on August 17, 2025 at 9:35am

Easy Way to Remove Microplastics From Your Drinking Water

Comment by Dr. Krishna Kumari Challa on August 16, 2025 at 9:21am

How gut microbiota makes genetically identical mice go different ways structurally and functionally while dealing with immune system

Genetically identical, but not the same: How gut microbiota composition shapes the immune system in mice

Laboratory mice are often considered the scientific equivalent of identical twins—genetically identical and expected to look and behave the same. But new research shows that this assumption doesn't always hold true. Researchers discovered that the composition of the gut microbiota can dramatically influence the structure and function of the immune system—even in genetically identical animals.

Researchers were surprised by how much the absence of microbiota increased phenotypic variability. Germ-free mice were each a little different, while those with a normal microbiota were much more alike.

They found that mice with a complex microbiota were more similar to each other than GF or OMM12-colonized mice, and the absence of microbiota dramatically increased variability in the shape and size of gut immune organs. While OMM12 partly restored gut morphology, it failed to restore physiological immune cell numbers or fully replicate the functional immune status of conventional mice.
Along the way, the team also described a previously unknown immune structure—the immunovillus. This densely immune cell–packed villus-like projection was found mainly in mice with restricted microbiota and may represent an adaptation to a specific microbial environment.

Published in the journal Gut Microbes, the study highlights the need to consider microbial context—not just genetics—when interpreting results from laboratory mouse models. Standardizing microbiota is essential for reproducibility, but current simplified microbial consortia such as OMM12 are not yet a perfect substitute for a natural complex microbiota.

Pačes Jan et al, Microbiota modulate immune cell populations and drive dynamic structural changes in gut-associated lymphoid tissue, Gut Microbes (2025). DOI: 10.1080/19490976.2025.2543908

Comment by Dr. Krishna Kumari Challa on August 16, 2025 at 9:09am

Balancing the immune system

When in working balance, the immune system protects the body against outside invaders without attacking its own tissues. B-cells release antibodies that attack pathogens and infected cells. Regulatory T-cells, or Tregs, keep the immune response from going too far, preventing tissue damage and autoimmune diseases.

When you prick your finger, it is important to mount a strong immune response to kill all the bacteria that entered your finger. But it's also important to bring that immune response to a halt when all the bacteria have been killed. Otherwise, you could lose your finger in the process, and the cure would be as bad as the disease.

A key target for B-cells are human leukocyte antigen (HLA) proteins, which help the immune system to tell self from non-self. Doctors try to match donor and recipient HLA proteins as closely as possible, but with more than 40,000 HLA variants, perfect matches are rare.

One variant, HLA-A2, is found in nearly one-third of the global population. Patients who have had previous exposure to HLA-A2 are considered "pre-sensitized," meaning their immune systems are primed to respond to it and release very large amounts of anti-HLA-A2 antibodies.

These include previous transplant patients; women who, during pregnancy, carried a child with HLA-A2 inherited from their partners; and recipients of HLA-A2-positive blood transfusions. Pre-sensitized patients have a much more difficult time finding a compatible donor organ.
In this new work, researchers developed a novel way for the Tregs to find and neutralize specifically the B-cells producing anti-HLA-A2 antibodies. They have fitted the Tregs with a CHAR—short for chimeric anti-HLA antibody receptor—which detects the appropriate B-cells and alerts the Tregs to suppress them.

When CHARs detect and attach to B-cells secreting anti-HLA-A2 antibodies, they alert the Tregs to neutralize these problematic B-cells, essentially signaling the immune system to stand down and not attack the organ. In this way, not only do CHARs act like heat-seeking missiles to find the right B-cells to target, but they also hold the key to the Treg's ignition, activating its machinery to elicit a more precise immunosuppressive response and prevent it from going overboard.
Researchers now took patients' cells that have been shown to make an extremely strong response against HLA-A2-expressing cells, and showed that the novel CHAR-Tregs calmed them down.

Chimeric anti-HLA antibody receptor engineered human regulatory T cells suppress alloantigen-specific B cells from pre-sensitized transplant recipients.v, Frontiers in Immunology (2025). DOI: 10.3389/fimmu.2025.1601385

Part 2

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Comment by Dr. Krishna Kumari Challa on August 16, 2025 at 9:05am

Genetically modified immune cell could help organ transplant patients who are prone to rejection

A medical research team  reports in Frontiers in Immunology that it has engineered a new type of genetically modified immune cell that can precisely target and neutralize antibody-producing cells complicit in organ rejection.

Similar strategies have been used to stimulate the immune system against certain cancers, but this research team is the first to show its utility in tamping down immune responses that can lead to organ rejection.

While often lifesaving, these organ transplant procedures depend on a precise match between donor and recipient genes to avoid rejection. When the immune system detects foreign tissue, it can attack the transplanted organ.

For decades, doctors have used immunosuppressant drugs to lower the risk of rejection. But these drugs work broadly, suppressing the entire immune system. This can lead to side effects and shorten the life of the transplanted organ.

This new work showed the feasibility of targeted immunosuppression after transplant that could one day reduce rejection without leaving patients vulnerable to infection and other side effects. This strategy could also level the playing field for patients who have limited eligibility for organs because they are especially prone to rejection.

Part 1

Comment by Dr. Krishna Kumari Challa on August 16, 2025 at 9:00am

Bioengineered platform uses bacteria to sneak viruses into tumors

Researchers have built a cancer therapy that makes bacteria and viruses work as a team. In a study published in Nature Biomedical Engineering, the Synthetic Biological Systems Lab shows how their system hides a virus inside a tumor-seeking bacterium, smuggles it past the immune system, and unleashes it inside cancerous tumors.

The new platform combines the bacteria's tendency to find and attack tumors with the virus's natural preference for infecting and killing cancerous cells.

The researchers think that this technology—validated in mice—represents the first example of directly engineered cooperation between bacteria and cancer-targeting viruses.

The approach combines the bacteria's instinct for homing in on tumors with a virus's knack for infecting and killing cancer cells.

By bridging bacterial engineering with synthetic virology, the goal is to open a path toward multi-organism therapies that can accomplish far more than any single microbe could achieve alone.

The researchers, therefore,  programmed the bacteria to act as an invisibility cloak, hiding the virus from circulating antibodies, and ferrying the virus to where it is needed. This  system demonstrates that bacteria can potentially be used to launch an oncolytic virus to treat solid tumors in patients who have developed immunity to these viruses.

Singer, Z.S., et al. Engineered bacteria launch and control an oncolytic virus, Nature Biomedical Engineering (2025). DOI: 10.1038/s41551-025-01476-8 www.nature.com/articles/s41551-025-01476-8

Comment by Dr. Krishna Kumari Challa on August 16, 2025 at 8:51am

Genetic study shows that common blood cancer includes subtypes

A new study  published in Cell Reports Medicine shows that follicular lymphoma (FL), a common type of blood cancer, is not one single disease but consists of three genetically distinct subtypes. The findings may help doctors diagnose and treat patients more accurately in the future.

Follicular lymphoma (FL) is a slow-growing cancer that affects white blood cells. Until now, it has been treated as one disease. However, by analyzing tumor samples from patients using whole-genome and transcriptomic sequencing, researchers  found that FL comprises three subtypes with distinct genetic profiles, biological features, and clinical outcomes.

These subtypes differ in how they develop and may respond differently to treatment. This means that patients could benefit from more personalized care based on the specific characteristics of their cancer, say the researchers.

The study employed advanced computational methods to investigate patterns in DNA mutations, gene expression, and immune cell behavior. The results showed that each subtype has its own cell of origin and interacts differently with the surrounding tissue. This could affect how the disease progresses and how well it responds to therapy.

Weicheng Ren et al, Whole-genome sequencing reveals three follicular lymphoma subtypes with distinct cell of origin and patient outcomes, Cell Reports Medicine (2025). DOI: 10.1016/j.xcrm.2025.102278

Comment by Dr. Krishna Kumari Challa on August 16, 2025 at 8:47am

Scientist uncover hidden immune 'hubs' that drive joint damage in rheumatoid arthritis

Rheumatoid arthritis (RA) is an autoimmune disease that affects millions worldwide and can have a devastating impact on patients' lives. Yet, about one in three patients respond poorly to existing treatments.

Researchers have shed new light on this challenge by discovering that peripheral helper T cells (Tph cells), a key type of immune cell involved in RA, exist in two forms: stem-like Tph cells and effector Tph cells. The stem-like Tph cells reside in immune "hubs" called tertiary lymphoid structures within inflamed joints, where they multiply and activate B cells.

Some of these then become effector Tph cells that leave the hubs and cause inflammation. This continuous supply of effector Tph cells may explain why inflammation persists in some patients despite treatment.

Targeting the stem-like Tph cells at the source could offer a new therapeutic strategy, bringing hope for more effective symptom relief and improved quality of life for patients living with RA.

The findings are published online in Science Immunology.

Yuki Mauso et al, Stem-like and effector peripheral helper T cells comprise distinct subsets in rheumatoid arthritis, Science Immunology (2025). DOI: 10.1126/sciimmunol.adt3955. www.science.org/doi/10.1126/sciimmunol.adt3955

Comment by Dr. Krishna Kumari Challa on August 16, 2025 at 8:44am

Dementia-like protein buildup found in pancreas cells before cancer develops

Multiple cancer types, including pancreatic cancer, are linked to a faulty mutation in a gene called KRAS, but scientists are increasingly learning that genetic changes are not the whole story.

Scientists have uncovered dementia-like behavior in pancreas cells at risk of turning into cancer. The findings provide clues that could help in the treatment and prevention of pancreatic cancer, a difficult-to-treat disease.

The research was published in the journal Developmental Cell in a paper titled "ER-phagy and proteostasis defects prime pancreatic epithelial state changes in KRAS-mediated oncogenesis."

Researchers studied pancreas cells in mice over time, to see what was causing healthy cells to turn into cancer cells. They discovered that pancreatic cells at risk of becoming cancerous, known as pre-cancers, develop faults in the cell's recycling process (known as "autophagy"). 

In pre-cancer cells, the researchers noticed excess "problem protein" molecules forming clumps—behavior seen in neurological diseases such as dementia. The researchers also noticed similar clumping occurring in human pancreas samples, suggesting this happens during pancreatic cancer development.

This  research shows the potential role autophagy disruption plays in the beginnings of pancreatic cancer. While early stage, we can potentially learn from research into other diseases where we see protein clumping, such as dementia, to better understand this aggressive type of cancer and how to prevent it.

One of the ways cells keep people healthy is by breaking down excess molecules they no longer need, through a recycling process called "autophagy." Autophagy is particularly important in the pancreas to control the level of digestive proteins and hormones the pancreas produces to help break down food.

Scientists have studied autophagy in detail over many years and are learning the key role it plays in diseases such as cancer. In some cases, cancer cells can become "addicted" to autophagy, hijacking the recycling process to help cancer cells divide and grow more quickly.

This research, on the other hand, suggests the combined effect of the faulty KRAS gene and disrupted autophagy could be driving the development of pancreatic cancer.

 ER-phagy and proteostasis defects prime pancreatic epithelial state changes in KRAS-mediated oncogenesis, Developmental Cell (2025). DOI: 10.1016/j.devcel.2025.07.016. www.cell.com/developmental-cel … 1534-5807(25)00473-3.

Comment by Dr. Krishna Kumari Challa on August 16, 2025 at 7:16am

How human protein ACE2 modulation could stop the entry of coronavirus

Early in the pandemic, most research focused on designing drugs that could block the virus's spike protein. This was a logical first step, but as we've seen, the virus is a moving target. It was rapidly evolving, and new variants acquired resistance due to changes in the surface spike glycoprotein (S protein).

This highlighted a critical challenge: would our treatments still work as the virus continued to change? Instead of constantly chasing new variants, scientists began to ask, what if they focused on how the human body responds to the virus, rather than only targeting the virus itself?

Instead of pursuing the virus directly, researchers decided to explore a new idea: targeting the human protein that mediates the virus's entry into cells in our body. This led them to angiotensin converting enzyme-2 (ACE2), the critical "gateway" protein the virus hijacks to begin its invasion. ACE2 is present on the surface of many human cells, especially in the lungs, and plays a crucial role in regulating blood pressure and heart health. Unfortunately, SARS-CoV-2 hijacks this protein as its entry point into cells.

This poses a significant challenge: blocking ACE2 entirely isn't a good option, as it's far too important for normal body functions. So the scientists' goal was: can they  make it harder for the virus to use ACE2 without disturbing its vital role in our bodies?

The researchers, in their experiments, found that when a suitable small molecule binds to  allosteric pocket of hACE2, it causes a conformational change in ACE2. This change primarily affects the global allostery, which is critical for the protein's interaction with the viral spike glycoprotein. This conformational shift weakens the binding between ACE2 and the viral spike protein, making it tougher for the virus to latch on and infect a cell.

The real innovation, however, is that this conformational change does not inhibit ACE2's normal function; in fact, their simulations and calculations confirmed that it enhances it.

Pratyush Pani et al, Modulating functional allostery of the host-cell receptor protein hACE2 to inhibit viral entry of SARS-CoV-2, Physical Chemistry Chemical Physics (2025). DOI: 10.1039/D5CP01740H

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