The Nobel Prize in medical science has been awarded for transformative discoveries that illuminate how the body's defense network attacks harmful infections while sparing the healthy tissues.
A trio of esteemed researchers—Japan's Shimon Sakaguchi and American experts Dr. Brunkow and Fred Ramsdell—received this honor.
The research uncovered specialized "sentinels" within the immune system that eliminate rogue defense cells capable of attacking the body.
These findings are now enabling new treatments for autoimmune diseases and malignancies.
These laureates will share a prize fund valued at 11m SEK.
"Their work has been decisive for understanding how the immune system functions and the reason we do not all suffer from severe autoimmune diseases," stated the head of the Nobel Committee.
The team's research address a core mystery: In what way does the defense system protect us from countless infections while leaving our own tissues unharmed?
Our immune system employs white blood cells that search for signs of disease, including viruses and germs it has not met before.
These cells utilize detectors—called receptors—that are generated randomly in countless variations.
That gives the immune system the capacity to combat a broad range of threats, but the unpredictability of the mechanism unavoidably produces white blood cells that may target the host.
Scientists earlier understood that a portion of these harmful defense cells were destroyed in the immune organ—where immune cells develop.
This year's Nobel Prize honors the discovery of T-reg cells—described as the immune system's "security guards"—which patrol the body 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.
A prize committee stated, "The findings have established a new field of research and spurred the creation of innovative therapies, for example for tumors and immune disorders."
In cancer, 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 under attack. A comparable approach could also be effective in reducing the risks of organ transplant rejection.
Prof Sakaguchi, of a Japanese institution, performed experiments on mice that had their thymus removed, leading to autoimmune disease.
He showed that introducing immune cells from healthy mice could stop the illness—implying there was a mechanism for preventing defenders from attacking the body.
Dr. Brunkow, from the a research center in Seattle, and Dr. Ramsdell, currently at a biotech firm in a California city, were investigating an genetic immune disorder in mice and humans that led to the discovery of a gene vital for how T-regs function.
"Their pioneering research has revealed how the body's defenses is kept in check by regulatory T cells, stopping it from mistakenly targeting the body's own tissues," commented a leading biological science specialist.
"The research is a remarkable illustration of how basic physiological research can have broad consequences for public health."
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