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

A trio of renowned scientists—Japan's Prof. Sakaguchi and American scientists Dr. Brunkow and Dr. Ramsdell—share this honor.

The work uncovered specialized "sentinels" within the immune system that remove rogue defense cells that could attacking the body.

These findings are now paving the way for new treatments for autoimmune diseases and malignancies.

These laureates will divide a prize fund valued at 11m SEK.

Decisive Discoveries

"The work has been essential for understanding how the body's defenses operates and the reason we don't all suffer from severe autoimmune diseases," stated the chair of the award panel.

The trio's research address a fundamental question: How does the defense system defend us from numerous infections while leaving our own tissues intact?

Our immune system employs white blood cells that scan for signs of infection, even viruses and germs it has never encountered.

Such defenders employ detectors—called receptors—that are generated by chance in a vast number of combinations.

This provides the immune system the capacity to combat a wide array of invaders, but the unpredictability of the process unavoidably produces immune cells that can attack the host.

Security Guards of the Immune System

Scientists previously understood that some of these harmful white blood cells were eliminated in the immune organ—the site where white blood cells develop.

This year's Nobel Prize honors the identification of regulatory T-cells—described as the body's "security guards"—which travel through the system to neutralize other defenders that attack the body's own tissues.

It is known that this mechanism fails in self-attack conditions such as type-1 diabetes, multiple sclerosis, and RA.

The Nobel panel added, "These discoveries have laid the foundation for a new field of research and accelerated the development of innovative therapies, for example for tumors and immune disorders."

In malignancies, T-regs prevent the body from attacking the tumor, so research are aimed at reducing their quantity.

For autoimmune diseases, experiments are testing increasing T-reg cells so the organism is not being harmed. A comparable method could also be useful in reducing the risks of transplanted organ rejection.

Innovative Experiments

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

He showed that introducing defense cells from other animals could prevent the illness—suggesting there was a mechanism for preventing immune cells from harming the body.

Dr. Brunkow, affiliated with the Institute for Systems Biology in Seattle, and Fred Ramsdell, currently at a biotech firm in San Francisco, were studying an inherited autoimmune disease in mice and humans that resulted in the identification of a genetic factor vital for how T-regs operate.

"Their pioneering research has revealed how the immune system is kept in check by T-reg cells, preventing it from mistakenly targeting the body's own tissues," commented a leading physiology specialist.

"This research is a remarkable illustration of how basic physiological research can have broad implications for public health."