The Nobel Prize in Physiology or Medicine has been awarded for transformative findings that illuminate how the immune system attacks harmful pathogens while sparing the healthy tissues.
A trio of renowned scientists—Japan's Shimon Sakaguchi and US experts Mary Brunkow and Fred Ramsdell—received this accolade.
Their work uncovered specialized "security guards" within the immune system that eliminate malfunctioning immune cells capable of attacking the organism.
The findings are now paving the way for innovative therapies for autoimmune diseases and malignancies.
The winners will share a monetary award valued at 11 million Swedish kronor.
"Their research has been essential for understanding how the immune system functions and why we don't all suffer from serious self-attack conditions," commented the head of the award panel.
This team's studies explain a core question: How does the defense system defend us from countless invaders while leaving our healthy cells intact?
Our immune system uses white blood cells that search for indicators of infection, including viruses and germs it has never encountered.
These cells employ sensors—called recognition units—that are generated by chance in a vast number of variations.
This provides the immune system the capacity to fight a broad range of invaders, but the unpredictability of the process unavoidably creates white blood cells that may attack the host.
Scientists earlier understood that some of these harmful white blood cells were eliminated in the immune organ—where immune cells mature.
The latest Nobel Prize honors the discovery of regulatory T-cells—known as the body's "peacekeepers"—which patrol the body to disarm other defenders that attack the body's own tissues.
We know that this mechanism malfunctions in autoimmune diseases such as type-1 diabetes, MS, and rheumatoid arthritis.
The prize committee stated, "These findings have established a new field of research and spurred the creation of new treatments, for example for tumors and immune disorders."
Regarding malignancies, regulatory T-cells prevent the system from fighting the tumor, so research are aimed at reducing their quantity.
For autoimmune diseases, trials are exploring boosting regulatory T-cells so the body is not under attack. A similar method could also be useful in reducing the risks of transplanted organ failure.
Professor Sakaguchi, of Osaka University, performed experiments on mice that had their immune gland removed, causing self-attack conditions.
He showed that introducing defense cells from healthy mice could stop the disease—suggesting there was a mechanism for blocking defenders from harming the body.
Mary Brunkow, affiliated with the Institute for Systems Biology in a US city, and Dr. Ramsdell, now at a biotech firm in San Francisco, were investigating an genetic immune disorder in rodents and humans that led to the identification of a gene vital for the way regulatory T-cells operate.
"Their pioneering research has revealed how the body's defenses is controlled by regulatory T cells, preventing it from accidentally targeting the healthy cells," said a prominent physiology expert.
"This work is a remarkable example of how fundamental biological research can have broad consequences for public health."
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