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This year's Nobel Prize in Physiology or Medicine was awarded for transformative discoveries that illuminate how the immune system targets dangerous infections while protecting the healthy tissues.

A trio of esteemed researchers—Japan's Shimon Sakaguchi and American experts Dr. Brunkow and Fred Ramsdell—share this honor.

The research identified specialized "sentinels" within the immune system that remove malfunctioning immune cells capable of harming the organism.

These findings are now paving the way for new treatments for immune disorders and malignancies.

These laureates will share a prize fund worth 11m Swedish kronor.

Crucial Discoveries

"The work has been essential for understanding how the body's defenses functions and the reason we don't all develop serious self-attack conditions," commented the head of the Nobel Committee.

This trio's research address a core question: In what way does the defense system defend us from numerous invaders while keeping our own tissues intact?

Our immune system uses white blood cells that search for signs of disease, even viruses and bacteria it has never encountered.

These defenders utilize detectors—known as receptors—that are generated randomly in a vast number of variations.

That provides the defense network the ability to combat a broad range of threats, but the unpredictability of the process unavoidably creates white blood cells that can attack the body.

Security Guards of the Body

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

The latest award honors the identification of T-reg cells—described as the body's "peacekeepers"—which travel through the body to disarm any defenders that attack the healthy cells.

It is known that this process malfunctions in self-attack conditions such as juvenile diabetes, multiple sclerosis, and rheumatoid arthritis.

A prize committee added, "These findings have established a novel area of research and spurred the development of innovative therapies, for example for tumors and autoimmune diseases."

In malignancies, T-regs block the system from attacking the tumor, so studies are aimed at reducing their quantity.

For self-attack disorders, experiments are testing increasing regulatory T-cells so the body is not being harmed. A comparable approach could also be effective in reducing the chances of organ transplant failure.

Innovative Studies

Prof Sakaguchi, of a Japanese institution, conducted experiments on mice that had their immune gland removed, causing autoimmune disease.

He demonstrated that introducing immune cells from other mice could prevent the disease—implying there was a mechanism for preventing immune cells from attacking the host.

Dr. Brunkow, affiliated with the Institute for Systems Biology in Seattle, and Dr. Ramsdell, now at Sonoma Biotherapeutics in a California city, were investigating an genetic autoimmune disease in mice and humans that resulted in the identification of a genetic factor critical for the way T-regs operate.

"The groundbreaking work has uncovered how the immune system is controlled by regulatory T cells, preventing it from mistakenly attacking the healthy cells," commented a leading physiology expert.

"The work is a striking example of how fundamental biological research can have broad consequences for human health."