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Autoreactive B cells have a major function in autoimmunity. A small subset of B cells expressing two distinct B-cell-antigen-receptors (B 2R  cells) is elevated in many patients with systematic lupus erythematosus (SLE) and in the MRL(/ lpr ) mouse model of lupus, and is often autoreactive. Here we show, using RNAseq and in vitro and in vivo analyses, signals that are required for promoting B 2R  cell numbers and effector function in autoimmune mice. Compared with conventional B cells, B 2R  cells are more responsive to Toll-like receptor 7/9 and type I/II interferon treatment, display higher levels of MHCII and co-receptors, and depend on IL-21 for their homeostasis; moreover they expand better upon T cell-dependent antigen stimulation, and mount a more robust memory response, which are characteristics essential for enhanced (auto)immune responses. Our findings thus provide insights on the stimuli for the expansion of an autoreactive B cell subset that may contribute to the etiology of SLE.

Innate and adaptive signals enhance differentiation and expansion of dual-antibody autoreactive B cells in lupus