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This year's prestigious award in medical science has been awarded for transformative discoveries that clarify how the body's defense network attacks harmful pathogens while sparing the healthy tissues.
A trio of esteemed researchers—from Japan Shimon Sakaguchi and US experts Mary Brunkow and Fred Ramsdell—received this accolade.
Their work uncovered specialized "sentinels" within the defense system that remove rogue defense cells that could attacking the body.
These findings are now enabling new treatments for autoimmune diseases and malignancies.
These laureates will share a monetary award worth 11m SEK.
"Their research has been decisive for comprehending how the immune system operates and why we don't all develop severe self-attack conditions," stated the head of the Nobel Committee.
This trio's studies explain a fundamental mystery: In what way does the defense system protect us from numerous infections while leaving our own tissues intact?
The body's protection system uses immune cells that search for indicators of infection, even viruses and bacteria it has never encountered.
Such defenders employ sensors—known as recognition units—that are produced randomly in countless variations.
This gives the defense network the ability to combat a broad range of invaders, but the randomness of the mechanism inevitably creates immune cells that can target the body.
Researchers earlier knew that some of these problematic white blood cells were destroyed in the thymus—the site where immune cells mature.
The latest Nobel Prize recognizes the discovery of T-reg cells—described as the body's "security guards"—which patrol the system to disarm any defenders that attack the body's own tissues.
We know that this mechanism fails in autoimmune diseases such as type-1 diabetes, multiple sclerosis, and rheumatoid arthritis.
The Nobel panel added, "These findings have established a novel area of research and spurred the development of new therapies, for instance for cancer and immune disorders."
In malignancies, T-regs prevent the system from fighting the growth, so studies are aimed at reducing their quantity.
For self-attack disorders, experiments are exploring increasing regulatory T-cells so the body is no longer under attack. A comparable approach could also be useful in reducing the risks of transplanted organ rejection.
Professor Shimon Sakaguchi, of Osaka University, performed tests on mice that had their immune gland extracted, causing autoimmune disease.
The researcher showed that introducing immune cells from other animals could prevent the disease—implying there was a mechanism for blocking defenders from harming the host.
Dr. Brunkow, affiliated with the a research center in a US city, and Dr. Ramsdell, currently at a biotech firm in a California city, were studying an genetic autoimmune disease in rodents and humans that resulted in the discovery of a genetic factor critical for the way regulatory T-cells operate.
"The groundbreaking work has uncovered how the body's defenses is kept in check by regulatory T cells, stopping it from mistakenly targeting the healthy cells," said a leading biological science expert.
"The research is a remarkable illustration of how basic biological study can have far-reaching implications for human health."
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