系统性红斑狼疮(Systemic lupus erythematosus, SLE)是以多器官、多系统受累为特点的自身免疫性疾病。目前的研究发现，SLE患者体内细胞过度凋亡和机体对凋亡细胞的清除障碍是启动SLE发病和疾病进展的重要因素之一。天然IgM（nIgM）在凋亡细胞的清除中发挥关键作用，有助于防止凋亡细胞诱导异常的自身免疫。Innate-like B细胞（ILBs）通过分泌nIgM发挥免疫调节功能，在自身免疫性疾病发病中起到保护作用。我们前期研究发现在SLE患者中，ILBs细胞数量明显减少且与疾病活动度呈负相关。本研究拟比较SLE患者与健康对照人群的ILBs细胞数量，ILBs细胞分泌nIgM的能力及nIgM结合多种抗原的能力，并分析SLE患者与健康对照ILBs细胞BCR受体库的差异，探讨SLE患者ILBs细胞减少及凋亡细胞清除障碍的可能机制，为寻求SLE新的治疗靶标做深入的探索。

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by multiple organ and system involvements. Present evidence found that apoptotic cells significant increased in SLE patients, and they seemed to have clearance disorder in the onset and progression of SLE. Natural IgM (nIgM) plays a key role in the clearance of apoptotic cells and prevents apoptotic cells from inducing abnormal autoimmunity. Innate-like B cells (ILBs) can play a protective role in autoimmune diseases by secreting nIgM to regulate immune function. Our previous study indicated that the proportion of ILBs in SLE patients decreased, which was negatively correlated with disease activity. The aim of the study is to compare the number of ILBs cells in SLE patients and healthy controls, the nIgM secreting ability of ILBs cells and ability of nIgM binding to multiple antigens. In addition, we analysis of the difference of BCR receptor Library of ILBs cells in SLE patients and healthy controls. Our study explores the possible mechanism of ILBs cell reduction as well as the clearance disorder of apoptotic cells in SLE patients to seek novel targets for SLE therapy.