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Significance The paradoxical coexistence of excessive autoantibodies and inadequate affinity-matured pathogen-specific antibodies in lupus is poorly understood. Here, we found that excessive CD11c+ T-bet+ age-associated B cells (ABCs)—a recently described autoimmunity-relevant B cell subset [K. Rubtsovaet al. ,J. Clin. Invest. 127, 1392–1404 (2017)]—not only contribute to the production of autoantibodies but also promote aberrant follicular T-helper (TFH ) cell differentiation and consequently compromise affinity-based germinal center (GC) B-cell selection and antibody-affinity maturation in lupus mouse models. Importantly, ablating B cell-intrinsic Toll-like receptor (TLR) signaling adaptor MyD88 in lupus mice inhibited CD11c+ T-bet+ ABC differentiation, normalized TFH differentiation, and rescued GC selection, as well as prevented autoantibody production, suggesting that CD11c+ T-bet+ ABCs and TLR signaling are potential targets for lupus treatment.

proceedings of the national academy of sciences of the united states of america

Excessive CD11c + Tbet + B cells promote aberrant T FH differentiation and affinity-based germinal center selection in lupus