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The Nobel Prize in medical science has been granted for transformative discoveries that clarify how the immune system attacks dangerous infections while sparing the body's own cells.

Three esteemed researchers—from Japan Prof. Sakaguchi and American scientists Mary Brunkow and Fred Ramsdell—share this accolade.

The work uncovered specialized "sentinels" within the immune system that eliminate rogue immune cells capable of harming the organism.

The findings are now enabling innovative treatments for autoimmune diseases and malignancies.

These winners will divide a prize fund worth 11m SEK.

Crucial Discoveries

"The work has been decisive for understanding how the body's defenses functions and the reason we don't all suffer from severe autoimmune diseases," stated the head of the Nobel Committee.

This trio's research address a core mystery: In what way does the immune system protect us from numerous invaders while leaving our healthy cells unharmed?

The immune system uses immune cells that search for signs of infection, even viruses and germs it has not met before.

Such defenders utilize detectors—called receptors—that are generated randomly in countless variations.

This provides the immune system the capacity to fight a wide array of threats, but the randomness of the process unavoidably produces immune cells that can target the host.

Protectors of the Body

Scientists previously understood that some of these problematic defense cells were eliminated in the immune organ—where white blood cells mature.

This year's Nobel Prize recognizes the identification of regulatory T-cells—known as the immune system's "peacekeepers"—which patrol the system to neutralize other immune cells that assault the healthy cells.

We know that this process malfunctions in autoimmune diseases such as juvenile diabetes, multiple sclerosis, and RA.

A prize committee added, "The discoveries have established a novel area of research and accelerated the development of innovative treatments, for instance for tumors and immune disorders."

In malignancies, regulatory T-cells prevent the body from attacking the tumor, so studies are aimed at reducing their quantity.

For autoimmune diseases, experiments are exploring boosting regulatory T-cells so the organism is no longer under attack. A similar approach could also be useful in minimizing the risks of organ transplant failure.

Innovative Studies

Professor Sakaguchi, of Osaka University, performed tests on mice that had their thymus removed, leading to autoimmune disease.

The researcher demonstrated that introducing defense cells from other mice could prevent the illness—implying there was a mechanism for blocking defenders from harming the host.

Mary Brunkow, from the Institute for Systems Biology in Seattle, and Fred Ramsdell, now at a biotech firm in San Francisco, were investigating an inherited autoimmune disease in rodents and humans that led to the identification of a gene critical for the way T-regs function.

"The pioneering research has revealed how the immune system is controlled by T-reg cells, preventing it from mistakenly attacking the body's own tissues," commented a leading biological science specialist.

"This work is a striking illustration of how fundamental biological study can have far-reaching consequences for human health."