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• W2913741774 abstract "The microbiota of the intestine has recently become the basis for increasing the incidence of autoimmune diseases in developed countries due to its role in regulating the immune system and changes in the intestinal microbiota. Useful microorganisms produce factors that are systematically distributed and thus can affect inflammatory responses. Definitely, genetics cannot increase disorder explains a number of immune diseases in the last few decades, especially T1D, MS, and asthma. Failure to properly educate the immune system during puberty causes an imbalance in subtypes of T-cell support, such as a T-cell deficiency that is susceptible to autoimmune diseases. Molecular mimicry describes the activation of cross-reactive T cells that recognize both the pathogen-derived epitopes and the self-derived epitopes. Pathogen-derived epitopes are taken up by APC and presented to T cells. Activation of T cells results in the direct lysis of self-tissue or release of cytokines and chemokines that activate macrophages, which mediate self-tissue damage and provide help to pathogen-specific B cells. The subsequent release of self-tissue antigens and their uptake by APC perpetuates the autoimmune disease. It's comfortable to suggest how microbiota educates the immune system. It corrects it in response to diet, health, and antibiotics, and ultimately determines the maturity of the immune system. Regardless of the barriers, studies about microbiota and microbiotics confer new valves for autoimmunity and its diseases. It may be possible to prove the links between a particular biosecurity and a particular autoimmune disease. Identifying them may be new approaches to prevent or treat it. Microbiota can be one of the factors regulating the immune system and autoimmune diseases via a variety of strategies. © 2019 Elsevier Inc." @default.
• W2913741774 created "2019-02-21" @default.
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• W2913741774 date "2019-06-01" @default.
• W2913741774 modified "2023-09-24" @default.
• W2913741774 title "Probiotics can really cure an autoimmune disease?" @default.
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• W2913741774 doi "https://doi.org/10.1016/j.genrep.2019.100364" @default.
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