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Toll‐like receptor engagement stimulates anti‐snRNP autoreactive B cells for activation

Autoreactive B cells are the source of pathogenic autoantibodies (autoAb) in systemic lupus erythematosus (SLE). Previous studies have demonstrated that anti‐small nuclear ribonucleoprotein particles (snRNP) B cells from normal background mice tolerize T cells in the periphery and do not secrete autoAb. In this study, we examined whether these anti‐snRNP B cells can be activated for autoAb production by the engagement of Toll‐like receptors (TLR). Anti‐snRNP B cells proliferated vigorously and secreted abundant anti‐snRNP autoAb upon exposure to CpG or polyriboinosinic polyribocytidylic acid [poly (I:C)] in vitro. In addition, the costimulatory molecules CD80 and CD86 were up‐regulated. While both anti‐snRNP B cells and wild‐type B cells produced similar levels of IL‐6 and IL‐10, anti‐snRNP B cells secreted predominately IFN‐γ in response to CpG or poly (I:C) stimulation. Furthermore, we showed that in vivo engagement of TLR stimulated immature anti‐snRNP B cells to further differentiate and produce autoAb and form germinal centers. The activated anti‐snRNP B cells became expanded and migrated into the T‐B cell interface. Moreover, TLR engagement directly or indirectly activated autoreactive B cells via a CD4 T cell‐independent manner. These results provide in vitro and in vivo evidence that BCR/TLR co‐engagement promotes the activation of anti‐snRNP B cells for autoAb production.