Eisenberg Robert
Division of Rheumatology, University of Pennsylvania, Philadelphia 19104, USA.
Endocr Metab Immune Disord Drug Targets. 2006 Dec;6(4):345-50. doi: 10.2174/187153006779025757.
B cells play a central role in the pathogenesis of SLE. Not only do they make autoantibodies, but they can provide immunoregulatory controls of T cells, dendritic cells, and other B cells, in part through cytokine production. The availability of a chimeric monoclonal antibody that targets B cells has made it possible to treat SLE by B-cell depletion. Rituximab binds to the B-cell specific antigen CD20, and depletes B cells from the peripheral blood and lymphoid tissues. A growing number of anecdotal series and case reports suggest that rituximab may provide clinical benefit in SLE with acceptable toxicity, although the variability in responses of individual patients is not yet fully understood. Two large ongoing randomized controlled trials will determine the efficacy of rituximab in SLE, both renal and extra-renal, and will inform us better about the biology of the B cell in this disease and the effects of B-cell depletion.
B细胞在系统性红斑狼疮（SLE）的发病机制中起核心作用。它们不仅产生自身抗体，还能部分通过细胞因子的产生对T细胞、树突状细胞和其他B细胞提供免疫调节控制。一种靶向B细胞的嵌合单克隆抗体的出现使得通过清除B细胞来治疗SLE成为可能。利妥昔单抗与B细胞特异性抗原CD20结合，从外周血和淋巴组织中清除B细胞。越来越多的轶事系列报道和病例报告表明，利妥昔单抗可能在SLE中提供具有可接受毒性的临床益处，尽管个体患者反应的变异性尚未完全了解。两项正在进行的大型随机对照试验将确定利妥昔单抗在SLE（包括肾脏和肾外表现）中的疗效，并将使我们更好地了解该疾病中B细胞的生物学特性以及B细胞清除的效果。
