[pubmed] Roles of cytokines and T cells in the pathogenesis of myasthenia gravis

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Clin Exp Immunol. 2020 Nov 13. doi: 10.1111/cei.13546. Online ahead of print.

ABSTRACT

Myasthenia gravis (MG) is characterized by muscle weakness and fatigability caused by the presence of autoantibodies against the acetylcholine receptor (AChR) or the muscle-specific tyrosine kinase (MuSK). Activated T cells, B cells, and plasma cells, as well as cytokines, play important roles in the production of pathogenic autoantibodies and the induction of inflammation at the neuromuscular junction in MG. Many studies have focused on the role of cytokines and lymphocytes in anti-AChR antibody-positive MG. Chronic inflammation mediated by T helper 17 (Th17) cells, the promotion of autoantibody production from B cells and plasma cells by follicular Th (Tfh) cells, and the activation of the immune response by dysfunction of regulatory T (Treg) cells may contribute to the exacerbation of the MG pathogenesis. In fact, an increased number of Th17 cells and Tfh cells and dysfunction of Treg cells have been reported in patients with anti-AChR antibody-positive MG; moreover, the number of these cells was correlated with clinical parameters in patients with MG. Regarding cytokines, interleukin 17 (IL-17; a Th17-related cytokine), IL-21 (a Tfh-related cytokine), the B-cell activating factor (BAFF; a B-cell-related cytokine), and a proliferation-inducing ligand (APRIL; a B-cell-related cytokine) have been reported to be upregulated and associated with clinical parameters of MG. This review focuses on the current understanding of the involvement of cytokines and lymphocytes in the immunological pathogenesis of MG, which may lead to the development of novel therapies for this disease in the near future.

PMID:33184844 | DOI:10.1111/cei.13546


Source: https://pubmed.ncbi.nlm.nih.gov/3318484 ... 4&v=2.13.0