How NKG2D ligands trigger autoimmunity?

How NKG2D ligands trigger autoimmunity?
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DOI:
10.1016/j.humimm.2006.02.013
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发表时间:
2006-03-01
期刊:
影响因子:
2.7
通讯作者:
Caillat-Zucman, Sophie
Caillat-Zucman, Sophie
中科院分区:
医学4区
文献类型:
--
作者:
Caillat-Zucman, Sophie

文献摘要

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NK和CD8 T细胞在消除感染、转化或应激细胞中的功能与对自身的耐受性一起发生,这是防止自身免疫所必需的特性。NK受体配体的不适当表达,导致自身反应效应细胞的激活,因此可能触发或加剧自身免疫。我们在这里回顾了一些关于激活受体NKG2D及其MIC配体的最新数据,这些数据表明它们在一些自身免疫性疾病中具有有害作用。
The function of NK and CD8 T cells in the elimination of infected, transformed, or stressed cells occurs together with tolerance to self, a property that is essential to prevent autoimmunity. Inappropriate expression of NK receptor ligands, leading to activation of autoreactive effector cells, might therefore trigger or exacerbate autoimmunity. We review here some recent data on the activating receptor NKG2D and its MIC ligand, which are indicative of their detrimental roles in some autoimmune disorders.