This year's Nobel Prize in Physiology or Medicine was granted for transformative discoveries that clarify how the body's defense network targets harmful pathogens while protecting the body's own cells.
Three renowned researchers—from Japan Prof. Sakaguchi and American scientists Mary Brunkow and Fred Ramsdell—received this honor.
Their work uncovered specialized "security guards" within the immune system that remove rogue defense cells that could attacking the body.
The findings are now paving the way for new therapies for immune disorders and malignancies.
These winners will share a monetary award worth 11m SEK.
"The research has been essential for comprehending how the immune system functions and the reason we don't all suffer from serious self-attack conditions," commented the head of the Nobel Committee.
This team's research explain a core mystery: In what way does the defense system protect us from countless invaders while keeping our healthy cells intact?
Our body's protection system uses immune cells that scan for indicators of disease, even pathogens and bacteria it has not met before.
Such cells employ sensors—known as receptors—that are produced by chance in a vast number of variations.
That gives the defense network the ability to combat a wide array of threats, but the randomness of the process inevitably creates white blood cells that may attack the host.
Researchers previously understood that some of these harmful white blood cells were destroyed in the immune organ—the site where white blood cells mature.
This year's Nobel Prize honors the discovery of T-reg cells—described as the body's "security guards"—which travel through the body to neutralize other immune cells that assault the body's own tissues.
It is known that this process fails in self-attack conditions such as juvenile diabetes, MS, and RA.
The prize committee stated, "These discoveries have laid the foundation for a new field of investigation and accelerated the development of new therapies, for instance for cancer and autoimmune diseases."
In malignancies, regulatory T-cells prevent the system from attacking the growth, so studies are aimed at lowering their quantity.
For autoimmune diseases, experiments are exploring increasing T-reg cells so the organism is no longer being harmed. A similar method could also be effective in minimizing the risks of transplanted organ failure.
Professor Sakaguchi, of Osaka University, performed experiments on rodents that had their immune gland removed, leading to self-attack conditions.
He demonstrated that introducing immune cells from other mice could stop the illness—suggesting there was a mechanism for blocking defenders from harming the body.
Dr. Brunkow, from the a research center in a US city, and Fred Ramsdell, currently at a biotech firm in a California city, were studying an inherited immune disorder in mice and people that led to the identification of a gene critical for how regulatory T-cells function.
"The pioneering research has uncovered how the immune system is controlled by regulatory T cells, preventing it from accidentally 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 far-reaching implications for human health."