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- W3137389411 endingPage "102800" @default.
- W3137389411 startingPage "102800" @default.
- W3137389411 abstract "Myasthenia gravis (MG) is a T cell-driven, B cell-mediated and autoantibody-dependent autoimmune disorder against neuromuscular junctions (NMJ). Accumulated evidence has emerged regarding the role of innate immunity in the pathogenesis of MG. In this review, we proposed two hypothesis underlying the pathological mechanism. In the context of gene predisposition, on the one hand, Toll-like receptors (TLRs) pathways were initiated by viral infection in the thymus with MG to generate chemokines and pro-inflammatory cytokines such as Type I interferon (IFN), which facilitate the thymus to function as a tertiary lymphoid organ (TLO). On the another hand, the antibodies against acetylcholine receptors (AChR) generated by thymus then activated the classical pathways on thymus and neuromuscular junction (NMJ). Futher, we also highlight the role of innate immune cells in the pathogenic response. Finally, we provide some future perspectives in developing new therapeutic approaches particularly targeting the innate immunity for MG." @default.
- W3137389411 created "2021-03-29" @default.
- W3137389411 creator A5045268007 @default.
- W3137389411 creator A5063900372 @default.
- W3137389411 creator A5071779584 @default.
- W3137389411 date "2021-05-01" @default.
- W3137389411 modified "2023-09-26" @default.
- W3137389411 title "The role of innate immunity in myasthenia gravis" @default.
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