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Updated: Dec 27, 2025

The bm12 Inducible Model of Systemic Lupus Erythematosus SLE in C57BL/6 Mice
Published on: November 1, 2015
B cells control lupus autoimmunity by inhibiting Th17 and promoting Th22 cells
Ji Yang1, Xue Yang2,3, Luman Wang4
1Department of Dermatology, Zhongshan Hospital, Fudan University, Shanghai, China. yang.ji@zs-hospital.sh.cn.
Abstract:
B cells exert immunosuppressive effects and offer therapeutic potential for systemic lupus erythematosus (SLE), but the mechanism remains unclear. Here we analyzed the B cell regulation of Th17/Th22 cell differentiation in lupus and found that α-IgM- and α-CD40-activated B cells could inhibit Th17 and promote Th22 cell differentiation from naive T cells under Th17 cell culture conditions. B cell-induced Th22 cells demonstrated immunosuppressive effects and could decrease renal endothelial cell apoptosis in vitro. Moreover, activated B cell infusion relieved lupus injuries via IL-22 production in vivo. Mechanically, activated B cells affected Th17/Th22 cell differentiation by non-contact TNF-α secretion and mTOR activation. Finally, activated B cells could affect Th17/Th22 cell differentiation in human peripheral blood T cells. These data suggest that activated B cells might attenuate lupus autoimmunity by inhibiting Th17 but promoting Th22 cell differentiation, supporting B cell activation as a promising therapeutic for the treatment of lupus.
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