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T-cell apoptosis in autoimmune diseases: termination of inf lammation in the nervous system and other sites with specialized immune-defense mechanisms

机译:自身免疫性疾病中的T细胞凋亡:通过专门的免疫防御机制终止神经系统和其他部位的炎症

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摘要

We have studied T-cell apoptosis in animal models of human autoimmune disorders of the nervous system and in other tissues devoid of specialized immune-defense mechanisms. Our data suggest that the CNS has high potential for elimination of T-cell-dependent inflammation, whereas this mechanism is less effective in the PNS, and is almost absent in other tissues such as muscle and skin. Interestingly, several conventional and novel immunotherapeutic approaches, such as glucocorticosteroid and high-dose antigen therapy, induce T-cell apoptosis experiments suggest different scenarios for the mechanisms by which specific cellular and humoral elements in the nervous system synergize and sensitize T cells for apoptosis We also discuss regulatory, proapoptotic mechanisms, such as the Fas–FasL system and galectin-1, that have been utilized in other tissues to mediate immune protection.
机译:我们已经研究了人类神经系统自身免疫性疾病的动物模型以及其他缺乏专门免疫防御机制的组织中的T细胞凋亡。我们的数据表明,中枢神经系统具有消除T细胞依赖性炎症的巨大潜力,而这种机制在PNS中效果较差,而在其他组织(如肌肉和皮肤)中几乎不存在。有趣的是,几种常规和新颖的免疫治疗方法,例如糖皮质激素和大剂量抗原治疗,可诱导T细胞凋亡实验,提示神经系统中特定细胞和体液成分协同作用并使T细胞对细胞凋亡敏感的机制不同。还讨论了调节性促凋亡机制,例如Fas–FasL系统和galectin-1,已在其他组织中用于介导免疫保护。

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