It has long been assumed that the functions of B cells reflected the roles of antibodies. However, B cells also decisively influence immunity via antibody-independent mechanisms including the presentation of antigen to T cells and the secretion of cytokines. In fact, B cell depletion therapy improves the course of autoimmune diseases such as multiple sclerosis by removing pro-inflammatory cytokine-producing B cells rather than by reducing autoantibody levels. Remarkably, B cells can also produce anti-inflammatory cytokines, and subsequently suppress immunity, providing protection from autoimmune diseases while interfering with beneficial responses against pathogens and cancers. A major mediator of this B cell regulatory function is their secretion of IL-10. There is considerable interest in identifying the mechanisms inducing the expression of IL-10 in B cells during the course of their activation. Here, we review the molecular mechanisms controlling IL-10 expression in B cells, and the evidence that IL-10-producing B cells play a protective role in human autoimmune diseases, underlying the relevance of this immunosuppressive axis for therapy.

长期以来，人们一直认为B细胞的功能反映了抗体的作用。但是，B细胞也会通过以下方式决定性地影响免疫力不依赖抗体的机制，包括将抗原呈递给T细胞和分泌细胞因子。实际上，B细胞耗竭疗法通过去除产生促炎性细胞因子的B细胞而不是通过降低自身抗体水平来改善自身免疫性疾病（例如多发性硬化症）的病程。值得注意的是，B细胞还可以产生抗炎性细胞因子，并随后抑制免疫力，从而保护自身免受自身免疫性疾病的侵害，同时干扰针对病原体和癌症的有益应答。B细胞调节功能的主要介体是它们分泌的IL-10。鉴定在B细胞活化过程中诱导IL-10在B细胞中表达的机制引起了极大的兴趣。在这里，我们回顾了控制B细胞中IL-10表达的分子机制，