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The Nobel Prize in Physiology or Medicine has been granted for revolutionary discoveries that clarify how the body's defense network targets harmful infections while protecting the healthy tissues.

A trio of renowned scientists—Japan's Prof. Sakaguchi and US scientists Mary Brunkow and Dr. Ramsdell—share this accolade.

The research uncovered unique "sentinels" within the defense system that remove malfunctioning immune cells that could harming the organism.

These discoveries are now enabling innovative therapies for autoimmune diseases and cancer.

The laureates will divide a prize fund worth 11 million Swedish kronor.

Decisive Discoveries

"Their work has been decisive for understanding how the body's defenses functions and why we don't all suffer from severe autoimmune diseases," commented the chair of the award panel.

This trio's research address a core mystery: How does the immune system defend us from numerous invaders while leaving our own tissues unharmed?

The body's protection system uses immune cells that scan for indicators of disease, even pathogens and germs it has never encountered.

Such cells utilize detectors—called recognition units—that are produced randomly in countless variations.

This gives the defense network the capacity to fight a broad range of threats, but the randomness of the process unavoidably creates white blood cells that may attack the body.

Security Guards of the Body

Researchers previously knew that some of these problematic white blood cells were eliminated in the immune organ—where white blood cells develop.

This year's award honors the identification of regulatory T-cells—known as the body's "security guards"—which travel through the system to disarm other defenders that assault the healthy cells.

It is known that this mechanism malfunctions in autoimmune diseases such as type-1 diabetes, MS, and RA.

The prize committee stated, "The findings have established a novel area of research and spurred the development of innovative treatments, for example for tumors and immune disorders."

In malignancies, T-regs block the body from fighting the tumor, so research are aimed at lowering their quantity.

In autoimmune diseases, experiments are testing boosting regulatory T-cells so the organism is no longer being harmed. A similar method could also be effective in minimizing the risks of organ transplant failure.

Innovative Studies

Prof Shimon Sakaguchi, of Osaka University, conducted experiments on mice that had their immune gland extracted, causing self-attack conditions.

He demonstrated that injecting immune cells from other mice could prevent the disease—suggesting there was a mechanism for preventing defenders from harming the body.

Dr. Brunkow, affiliated with the Institute for Systems Biology in Seattle, and Dr. Ramsdell, currently at Sonoma Biotherapeutics in San Francisco, were studying an genetic immune disorder in mice and humans that led to the identification of a genetic factor vital for how regulatory T-cells function.

"Their groundbreaking research has uncovered how the immune system is controlled by regulatory T cells, stopping it from mistakenly targeting the healthy cells," said a leading biological science expert.

"This research is a striking example of how basic physiological study can have far-reaching implications for human health."