Scientists have found the memory of the immune system
Last reviewed: 23.04.2024
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The immune system has a type of cells that remind it not to attack cells, tissues and organs of its own organism, the UCSF researchers found.
According to UCSF scientists, this discovery is likely to lead to new strategies to combat a wide range of autoimmune diseases - in which the immune system attacks and destroys cells within one's own organism, as well as to prevent a rejection reaction of the transplant.
Cells identified by UCSF scientists circulate in the blood and are copies of memory cells that protect pathogenic microorganisms after vaccination or repeated exposure to the same pathogen.
To determine the role of memory cells, called activated T cells, in the work of the immune system, the UCSF immunologist and the head of the pathology department Abul Abbas used mice with autoimmune disease.
He found that over time, tissues in the body - in the study, the skin - protect themselves from autoimmune attacks by activating a small portion of the regulatory T-cells.
Autoimmune diseases, from minor to severe, affect approximately 50 million Americans. For many decades, immunologists believed that these diseases develop due to a defect in the functioning of immunocytes, known as lymphocytes, including cells that synthesize antibodies to pathogens of various kinds of diseases.
In autoimmune diseases, lymphocytes can be directed against their own proteins. For example, with multiple sclerosis, lymphocytes produce antibodies that attack the proteins of the myelin sheath that surrounds the nerves, with lupus - own DNA.
But in many cases, autoimmune diseases can be associated with an abnormal response of T-regulating cells, say UCSF researchers. In recent years, immunologists have come to understand the important role of T-regulating cells, which are associated not only with a decrease in the immune response during recovery from infection, but also in the prevention of autoimmune reactions.
UCSF researchers wanted to learn how an autoimmune reaction can self-limit or diminish over time. Doctors noticed that in many cases of autoimmune diseases, the first time the immune attack on the organs is more aggressive, compared with later outbreaks of the immune response.
UCSF scientists created a genetically engineered strain of mice in which they could turn on or turn off the production of a protein in the skin called ovalbumin, which would provoke an autoimmune response.
The presence of protein also stimulated the activation of T-regulating cells. When scientists again increased the production of ovalbumin in mice, it caused a weak autoimmune response, due to the already activated T cells.
Currently, T-regulating cells are already being studied in therapy aimed at preventing the rejection reaction of transplanted organs.
The discovery of long-lived memory cells in the T-regulating cell population indicates the enormous prospects of using specialized memory cells to prevent attacks on specific molecular targets that immunologists call "antigens."
Since the role of activated T-regulating memory cells has not been previously recognized, this study can be a major impetus for initiating clinical trials of the use of specific immunotherapy for multiple sclerosis and type 1 diabetes.
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