Nat Immunol: scientists are expected to develop new therapies for autoimmune diseases
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Last Update: 2020-01-09
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Source: Internet
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Author: User
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January 9, 2020 / biool / -- recently, in a research report published in the international journal Nature Immunology, scientists from Cincinnati Children's medical center and other institutions described a complete new molecular process in mice through research, which may induce T-cell-driven inflammation and trigger different autoimmunity Sexual diseases: the relevant research results have certain significance for the treatment of a variety of diseases, such as multiple sclerosis, 1-diabetes and inflammatory bowel disease, and also hope to help researchers find new therapies to treat autoimmune diseases Source: chandrashekhar pasare, researcher of Cincinnati Children's, said that we are currently testing the molecular processes found in a variety of human cells, and working with other researchers to collect cell samples from patients with multiple sclerosis, arthritis and other autoimmune diseases In the past 10 years, researchers believe that the immune system protein IL-1B (cytokine IL-1 - β) is related to a variety of autoimmune diseases Drugs and antibodies that block or inhibit IL-1B can be used to effectively control the disease status of patients with various types of autoimmune diseases Up to now, researchers have no idea how the body makes IL-1B, Especially during the autoimmune period, this may significantly limit the development of new therapies for autoimmune diseases Previously, researchers thought that the production of IL-1B needs to activate a group of immune system protein molecules, which can form inflammatory bodies Later, researchers found that inflammatory bodies can act as systematic sensors to activate inflammation, thus inducing so-called autoimmune diseases, which is different from autoimmune diseases Pasare and his colleagues found that, unlike inflammatory corpuscles, a different molecular pathway can accelerate the body's inflammatory response in the process of autoimmunity, which can be induced by the interaction between myeloid cells and CD4 positive T cells, thus helping to attack harmful bacteria , viruses and other microorganisms; fortunately, in the case of autoimmunity, the immune system can attack and destroy healthy tissues When IL-1B can't play the role of driving the autoimmune function, it is usually used as the stimulant of anti microbial immunity However, in the process of autoimmunity, researchers found that the other two molecules (TNF and FasL) can play the role of autoimmune T cells, macrophages and dendritic cells, so as to produce excessive IL-1B This means that our findings have some significance Firstly, IL-1B can also be produced when infection does not exist, and T cells can be the main driver of IL-1B in autoimmune condition The researchers pointed out that the therapy of targeting IL-1B produced by inflammatory corpuscles may have some limitations in the treatment of autoimmune diseases, which confirmed that the self reactive T cells have the self mechanism of driving inflammation, and they can play a role independently of inflammatory corpuscles TNF and FasL pathway in the process of IL-1B production may be expected to effectively treat human autoimmune diseases At last, the researchers emphasized that it is too early for the research results to be translated into the treatment of patients in the clinic, because the pre clinical research findings are obtained through the research of laboratory models; firstly, researchers need to conduct additional pre clinical research, and anti TNF therapy has been used in the clinical treatment of some autoimmune diseases, and Further blocking FasL may also be an effective treatment for autoimmune diseases, and later researchers will continue to conduct in-depth research in preclinical models for more tests Original sources: Jain, A., irizarry Caro, R.A., McDaniel, M.M et al T cell instrument myeloid cells to produce informsome independent IL-1 β and cause autoimmunity NAT immune 21, 65 – 74 (2020) doi: 10.1038/s41590-019-0559-y
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