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• W2068709938 abstract "Although IL-17 is considered to promote B cell differentiation into antibody-secreting plasma cells in some autoimmune diseases, its mechanism remains unclear. Recent studies revealed that autophagy, a lysosome-mediated catabolic process for providing nutrients under starvation, could regulate plasma cell homeostasis, so this study aimed to explore whether and how autophagy participates in IL-17-mediated plasma cell differentiation by MyHC-α-induced experimental autoimmune myocarditis (EAM) mouse model. It showed that IL-17 could not only induce B cell autophagy, but also facilitate the myocarditis severity, serum anti-MyHC-α autoantibody production and splenic CD38+ CD138+ B cell percentages, while the autophagy inhibitor 3-methyladenine attenuated these effects. Furthermore, serum anti-MyHC-α IgG autoantibody productions and CD38+ CD138+ B cell percentages were positively correlated with B cell autophagy levels respectively. In vitro, we further revealed that IL-17 could directly promote B cell autophagy, which boosted Blimp-1 expressions and CD38+ CD138+ B cell percentages. Moreover, elevated autophagy mediated by IL-17 enhanced ubiquitin–proteasome system activity and B cell anti-apoptotic ability by Beclin-1 and p62 through Erk1/2 phosphorylation, and these changes brought by IL-17 could be also inhibited with 3-methyladenine. Therefore, we concluded that autophagy contributed to IL-17-mediated plasma cell differentiation by regulating Blimp-1 expression and Beclin-1/p62 associated B cell apoptosis in EAM." @default.
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• W2068709938 date "2014-01-01" @default.
• W2068709938 modified "2023-10-15" @default.
• W2068709938 title "Autophagy contributes to IL-17-induced plasma cell differentiation in experimental autoimmune myocarditis" @default.
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• W2068709938 doi "https://doi.org/10.1016/j.intimp.2013.11.008" @default.
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