B cells are recognized as key participant in various autoimmune diseases, including systemic lupus erythematosus (SLE). Although sets of transcription factors and cytokines are known to regulate B cells differentiation, the roles of microRNAs are poorly understood. Our previous study has proved that microRNA-326 (miR-326) was markedly upregulated in SLE patients; however, the biological function of miR-326 during SLE pathogenesis remained unknown. In this study, we found that miR-326 overexpression in MRL/lpr mice led to B cell hyperactivity and severe SLE. Moreover, E26 transformation–specific-1 (Ets-1), a negative regulator of B cells differentiation, was identified as a target of miR-326. Therefore, a novel mechanism has been found in which the elevated miR-326 in B cells of SLE promotes plasmablasts development and antibody production through down-regulation of Ets-1.

B细胞被认为是包括系统性红斑狼疮（SLE）在内的各种自身免疫疾病的主要参与者。尽管已知转录因子和细胞因子集可调节B细胞分化，但人们对microRNA的作用了解甚少。我们之前的研究证明，SLE患者中的microRNA-326（miR-326）明显上调；然而，miR-326在SLE发病过程中的生物学功能仍然未知。在这项研究中，我们发现MRL / lpr小鼠中的miR-326过表达导致B细胞过度活跃和严重的SLE。此外，E26转化特异性1（Ets-1）是B细胞分化的负调节剂，被确定为miR-326的靶标。所以，