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• W2904993536 startingPage "305" @default.
• W2904993536 abstract "Summary The immune system is essential for maintaining a delicate balance between eliminating pathogens and maintaining tolerance to self‐tissues to avoid autoimmunity. An enormous and complex community of gut microbiota provides essential health benefits to the host, particularly by regulating immune homeostasis. Many of the metabolites derived from commensals can impact host health by directly regulating the immune system. Many autoimmune diseases arise from an imbalance between pathogenic effector T cells and regulatory T (Treg) cells. Recent interest has emerged in understanding how cross‐talk between gut microbiota and the host immune system promotes autoimmune development by controlling the differentiation and plasticity of T helper and Treg cells. At the molecular level, our recent study, along with others, demonstrates that asymptomatic colonization by commensal bacteria in the gut is capable of triggering autoimmune disease by molecular mimicking self‐antigen and skewing the expression of dual T‐cell receptors on T cells. Dysbiosis, an imbalance of the gut microbiota, is involved in autoimmune development in both mice and humans. Although it is well known that dysbiosis can impact diseases occurring within the gut, growing literature suggests that dysbiosis also causes the development of gut‐distal/non‐gut autoimmunity. In this review, we discuss recent advances in understanding the potential molecular mechanisms whereby gut microbiota induces autoimmunity, and the evidence that the gut microbiota triggers gut‐distal autoimmune diseases." @default.
• W2904993536 created "2018-12-22" @default.
• W2904993536 creator A5013133770 @default.
• W2904993536 creator A5023729821 @default.
• W2904993536 creator A5026726785 @default.
• W2904993536 creator A5054827603 @default.
• W2904993536 date "2019-01-21" @default.
• W2904993536 modified "2023-10-05" @default.
• W2904993536 title "Impact of gut microbiota on gut‐distal autoimmunity: a focus on T cells" @default.
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