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首页> 外文期刊>Autoimmunity >T cell abnormalities in systemic lupus erythematosus.
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T cell abnormalities in systemic lupus erythematosus.

机译：系统性红斑狼疮中的T细胞异常。

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摘要

Because of the consensus that T cells play a central role in the pathogenesis of systemic lupus erythematosus (SLE), we explored the molecular basis of the defective function of SLE T cells for expression of signal transduction molecules, as well as surface structures such as adhesion molecules, by extensively testing peripheral blood T cells from SLE patients. Upregulated expression and function of adhesion molecules was observed in T cells from patients with active SLE who had specific clinical manifestations such as vasculitis, epithelitis and arthritis, but proximal signal transduction was defective. Comprehensive analysis to identify the molecules responsible for the defects showed the expression of the TCR zeta chain was attenuated, or absent in more than half of SLE patients. Moreover, the aberrant transcripts of the TCR zeta chain, including spliced variants lacking exon 7 and with a short 3' UTR, were detected in SLE T cells. Although attenuated expression of the TCR zeta chain is also observed in patients with cancers, infections and other autoimmune diseases, sustained attenuation of TCR zeta expression and aberrant transcripts are only observed in SLE. In this review we discuss the unique features of the TCR zeta defects in SLE.
机译：由于一致认为T细胞在系统性红斑狼疮（SLE）的发病机理中起着核心作用，因此我们探索了SLE T细胞表达信号转导分子以及表面结构（如黏附）的缺陷功能的分子基础。通过广泛测试SLE患者的外周血T细胞来检测这些分子。活动性SLE患者的T细胞中观察到粘附分子的表达和功能上调，这些患者具有特定的临床表现，如血管炎，上皮炎和关节炎，但近端信号传导存在缺陷。进行全面分析以鉴定造成缺陷的分子后，在一半以上的SLE患者中，TCR zeta链的表达减弱或缺失。此外，在SLE T细胞中检测到TCR zeta链的异常转录本，包括缺少外显子7和3'UTR短的剪接变体。尽管在患有癌症，感染和其他自身免疫性疾病的患者中也观察到TCR zeta链的表达减弱，但仅在SLE中观察到TCR zeta表达和异常转录物的持续减弱。在本文中，我们讨论了SLE中TCR zeta缺陷的独特特征。

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