Kyttaris Vasileios C, Krishnan Sandeep, Tsokos George C
Division of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02115, USA.
Autoimmunity. 2006 Dec;39(8):705-9. doi: 10.1080/08916930601061363.
Overactive B cells, abnormally activated T cells and inappropriate handling of cellular debris by the innate immune system are central in the pathogenesis of systemic lupus erythematosus (SLE). Genetic studies in SLE patients have unraveled allelic variations in genes encoding key molecules that control inter- and intra-cellular signaling and play a role in the abnormal handling of apoptotic material. Despite recent breakthroughs though, it is still unclear how exactly genes and environment interact to produce the characteristic immune dysregulation in SLE.
过度活跃的B细胞、异常活化的T细胞以及先天免疫系统对细胞碎片的不当处理在系统性红斑狼疮(SLE)的发病机制中起着核心作用。对SLE患者的基因研究揭示了编码关键分子的基因中的等位基因变异,这些关键分子控制细胞间和细胞内信号传导,并在凋亡物质的异常处理中发挥作用。尽管最近有了一些突破,但基因和环境究竟如何相互作用以产生SLE特有的免疫失调仍不清楚。