Mary E. Bronko, Farid Ramzel, and Simon Sakaguchi, Nobel Prize for the year 2025 in physiology or medicine, for their discoveries related to peripheral immune tolerance.
The Nobel Association at the Carolinska Institute said that these scientists were awarded the award because they discovered how to maintain the immune system under control.
Sakagucci is a prestigious professor at the Immunology Research Center at the University of Osaka in Japan. Bronco is also currently the position of first program director at the Systems Biology Institute in Seattle, while Ramuma is a scientific advisor for Sonoma Pioterpixus in San Francisco.
The Nobel Committee praised the work of the winners to motivate them to conduct clinical trials on possible new treatments, such as treatments that may activate immune cells called organizational T cells, which can curb excessive immune responses in autoimmune diseases or organ transplants.
What are the discoveries of the scholars that qualified them to obtain Nobel?
Our immune system protects us daily from thousands of different microbes that try to invade our bodies. Each has a different appearance, and many of them have developed similarities with human cells as a kind of camouflage. How does the immune system determine what it should attack and what it should defend.
The winners have identified organizational T cells, the guards of the immune system, which prevent immune cells from attacking our bodies.
“Their discoveries were decisive in our understanding of how the immune system was working and why not all have serious autoimmune diseases.”
Sakagucci was swimming in the opposite of the current in 1995, when he achieved the first important discovery. At that time, many researchers were convinced that immune tolerance was developing only as a result of the destruction of potential harmful immune cells in the thyme, through the “central endurance” process. Sakagucci showed that the immune system is more complicated, and discovered a previously unknown category of immune cells, which protects the body from autoimmune diseases.
Bronco and Amsdel also reached another important discovery in 2001, when they explained the reason that a certain breed of mice is more vulnerable to autoimmune diseases. They discovered that mice had a boom in a gene called “Foxp3”. They also showed that the mutations in the gene corresponding to this gene in humans caused a serious self -immune disease known as “IPEX”.
Two years later, Sakagucci was able to connect these discoveries, and it has proven that “FOXP3” controls the growth of the cells that he identified in 1995. These cells, now known as organizational T cells, monitor other immune cells and ensure the acceptance of our immune system for our tissues.
The discoveries of the award -winning have launched the field of peripheral endurance, which motivated the development of medical treatments for cancer and autoimmune diseases. This may also increase the success of organ transplants. Many of these treatments are currently undergoing clinical trials.
The human immune system is the basic defense line of our body against harmful microbes, viruses and other invaders, but it may sometimes get mad and attack healthy cells. This is the basis of many autoimmune diseases, from cancer to rheumatoid arthritis and type 1 diabetes. The Nobel Prize in this year’s physiology or medicine was awarded to scientists who conducted basic research on peripheral immune endurance, a system that discourages the immune system and prevents it from damaging the body.
“The Nobel Prize for this year is related to physiology or medicine how to keep our immune system under control so that we can fight all microbes that can be imagined and avoid autoimmune diseases,” says Marie and Aharrin Herleneus, a member of the Nobel Committee for the year 2025 in physiology or medicine, at a press conference broadcast directly today from Stockholm.
In the 1970s, scientists suggested for the first time the existence of a distinctive group of T -cells capable of inhibiting the immune response. It was believed that these cells, which were then known as glyabight T -cells, could open new horizons for understanding the immune system and autoimmune diseases. However, the first experiences that tried to prove the existence of these cells were unsuccessful, as this theory was eventually abandoned because they are very marginal.
In addition to the Nobel Prize -winning company, the immunity scientist, Jeffrey Blosson, said in a statement to the Scinvik American – that early research “has identified activities without a clear molecular understanding.” He added, “It was difficult to repeat some works, and therefore by the end of the contract, many questioned the existence of such a system,” he added.
Glacate T cells
Years later, Sakagucci – who was then an immunity scientist at the Institute for the AICI Cancer Center in Nagoya, Japan – resumed working on the cakes. “The primary hope was the discovery of a distinctive molecular feature on the surface of these cells. It is a sign of the distinction of ti -cells that are captivated from other cells,” wrote in the 2006 article in the Scientific American magazine, with the participation of the immune scientist Zoltan Vehrafari and is now a first editor in Nature magazine.
Sakagucci and his colleagues focused on the thymus gland, a member located in the chest where the cells ripen and are taught to avoid targeting healthy cells. The thymus gland is supposed to eliminate any defective TV. But in some autoimmunes, these harmful elements can fly under the radar.
In a series of experiments on mice, Sakagucci found that the auxiliary cells produced with thymus gland (identified by the CD4 CD4 surface protein not all of them in the same way. Cells that contain an additional new surface protein seemed necessary to prevent the immune system from attacking the body itself.
In the experiments in which Sakaguchi and his colleagues wiped mice from the T -cells of “CD4”, various organs (thyroid, stomach, gonads, pancreas, and salivary glands) surrendered to white blood cell attacks, and led to “acute inflammation” as Sakaguchi and Vehrafari wrote in the magazine of the American.
The discovery of the CD25 (CD25) – which was first detailed in a major research paper in 1995 in the Hunger’s Magazine – Sakagucci to create a new category of T -cells, which was called organizational T cells.
“It was not a prominent research paper at the time. He was devoting his efforts to publishing a research paper after another on this topic to refine its results,” says Peter Savage, a professor of pathology at the University of Chicago, who studies organizational T cells. “The idea of glyted cells had lost its popularity. It was Sakagucci who sought this idea, through a series of accurate experiences, and was able to determine a group of T -cells CD4 with a strong captivating activity or (Hafiz Al Salam) activity.”
In Washington State, Bronko and Amsdel strengthened the role of T -regulatory cells in the activity of the immune system through several research papers published in 2001 that dealt with the genetic foundations of the cells.
To find out if this “peacekeeping” cells are a unique breed of T -cells or just a passing group, Ramsaled and Bronco studied mice infected with dandruff, a strain that was born unexpectedly with scrub leather and a swollen lymph nodes that lived only a few weeks.
By analyzing genes in healthy and dandruff mice, the team identified a mutamorine called “OXP3” as the main gene responsible for autoimmune in sick mice. The researchers later found that the mutations of this gene caused an acute autoimmune disease called “IPEX” (IPEX), which means immune disorder, multi -endocrine disease, intestinal illness, and syndrome associated with chromosome “X” in humans.
These genetic results paved the way for Sakagucci, and researchers in other laboratories, to confirm that “FOXP3” controls the development of T -regulatory cells.