snrnp自身反应性狼疮T细胞克隆异常早期TCR/ cd3介导的信号事件

Stamatis-Nick C. Liossis , Robert W. Hoffman , George C. Tsokos
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引用次数: 22

摘要

多发性免疫调节异常是系统性红斑狼疮的特征。抗原受体介导的早期信号转导生化事件的异常强调了细胞畸变的多样性。来自系统性红斑狼疮患者的新鲜外周血T细胞和B细胞以及T细胞系显示出增加的Ca2+反应,这是在抗原受体启动的细胞质蛋白酪氨酸磷酸化增强之前。为了进一步剖析狼疮T细胞的异常信号事件,我们研究了狼疮患者自身抗原特异性T细胞中抗cd3单克隆抗体诱导的早期信号事件。我们在此报道狼疮snrnp特异性T细胞克隆,而不是其他T细胞,在TCR/CD3刺激后显示出增加的Ca2+通量和增强的酪氨酸磷酸化蛋白的产生。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Abnormal Early TCR/CD3-Mediated Signaling Events of a snRNP-Autoreactive Lupus T Cell Clone

Multiple immunoregulatory abnormalities characterize systemic lupus erythematosus. Abnormalities of the antigen receptor-mediated early signal transduction biochemical events underscore the diverse cellular aberrations. Fresh peripheral T and B cells and T cell lines from patients with systemic lupus erythematosus display increased Ca2+responses that are preceded by enhanced antigen receptor-initiated cytosolic protein tyrosine phosphorylation. To further dissect the aberrant signaling events of lupus T cells we studied the early anti-CD3 mAb-induced signaling events in autoantigen-specific T cells from lupus patients. We report herein that a lupus snRNP-specific T cell clone, but not other T cells, displays increased Ca2+fluxes and enhanced production of tyrosine-phosphorylated proteins following TCR/CD3 stimulation.

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