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系统性红斑狼疮(Systemic lupus erythematosus,SLE)是一种与环境和遗传因素相关的复杂性自身免疫系统疾病,以大量自身抗体产生、免疫复合物蓄积导致多系统损伤为特点。SLE的发病机制极为复杂,其中,以异常T细胞活化较为重要,因其引起细胞因子失衡,导致机体持续产生自身抗体和自身反应性T细胞。本文将以异常T细胞活化过程中的钙离子信号异常为核心,概述近年来SLE异常T细胞活化机制及其相关药物研究的新进展。
Systemic lupus erythematosus (SLE) is a complex and autoimmune disease associated with environmental and genetic factors characterized by massive autoantibodies and accumulation of immune complexes leading to multiple systemic injuries. The pathogenesis of SLE is extremely complex. Among them, abnormal T cell activation is more important because it causes imbalance of cytokines, resulting in the continuous production of autoantibodies and autoreactive T cells in the body. In this paper, we will focus on the aberrant signal transduction of Ca2 + in abnormal T cell activation and summarize the recent progress in the mechanism of SLE abnormal T cell activation and its related drugs.