This year's Nobel Prize in Physiology or Medicine has been awarded for transformative discoveries that illuminate how the immune system targets harmful infections while protecting the healthy tissues.
A trio of renowned researchers—from Japan Prof. Sakaguchi and US scientists Dr. Brunkow and Fred Ramsdell—share this honor.
The work uncovered specialized "security guards" within the immune system that remove rogue immune cells capable of harming the organism.
These discoveries are now paving the way for new therapies for immune disorders and cancer.
The laureates will share a monetary award valued at 11m SEK.
"The research has been essential for comprehending how the immune system functions and the reason we don't all develop severe autoimmune diseases," commented the chair of the award panel.
This team's research explain a fundamental question: In what way does the immune system protect us from countless infections while leaving our own tissues intact?
Our immune system employs immune cells that search for indicators of disease, including pathogens and germs it has not met before.
These defenders utilize detectors—called recognition units—that are produced randomly in a vast number of combinations.
That gives the defense network the ability to combat a broad range of threats, but the randomness of the mechanism inevitably produces white blood cells that may target the body.
Scientists previously understood that a portion of these problematic white blood cells were destroyed in the thymus—where immune cells develop.
The latest Nobel Prize honors the identification of regulatory T-cells—described as the body's "security guards"—which patrol the system to neutralize any immune cells that attack the healthy cells.
We know that this process fails in self-attack conditions such as juvenile diabetes, multiple sclerosis, and RA.
The prize committee added, "The discoveries have established a new field of investigation and spurred the development of new treatments, for instance for tumors and autoimmune diseases."
In malignancies, regulatory T-cells block the body from attacking the growth, so research are focused on lowering their quantity.
In self-attack disorders, trials are exploring increasing regulatory T-cells so the body is no longer under attack. A comparable approach could also be useful in minimizing the risks of transplanted organ rejection.
Prof Sakaguchi, of Osaka University, performed experiments on mice that had their thymus extracted, leading to autoimmune disease.
He showed that introducing defense cells from other animals could stop the illness—suggesting there was a system for preventing defenders from harming the host.
Mary Brunkow, from the Institute for Systems Biology in a US city, and Dr. Ramsdell, currently at a biotech firm in a California city, were investigating an genetic autoimmune disease in rodents and people that led to the discovery of a genetic factor critical for the way regulatory T-cells operate.
"The pioneering work has revealed how the body's defenses is controlled by T-reg cells, preventing it from mistakenly attacking the healthy cells," commented a leading physiology expert.
"The research is a remarkable illustration of how basic biological research can have broad consequences for public health."
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