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NKG2D配体如何引发自身免疫?

How NKG2D ligands trigger autoimmunity?

作者信息

Caillat-Zucman Sophie

机构信息

AVENIR Team INSERM U561, Hôpital St-Vincent de Paul, Paris, France.

出版信息

Hum Immunol. 2006 Mar;67(3):204-7. doi: 10.1016/j.humimm.2006.02.013. Epub 2006 Mar 31.

DOI:10.1016/j.humimm.2006.02.013
PMID:16698443
Abstract

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.

摘要

NK细胞和CD8 T细胞在清除受感染、发生转化或处于应激状态的细胞时发挥作用,同时具备对自身的耐受性,这一特性对于预防自身免疫至关重要。因此,NK受体配体的不适当表达导致自身反应性效应细胞的激活,可能会引发或加剧自身免疫。我们在此综述一些关于激活受体NKG2D及其MIC配体的最新数据,这些数据表明它们在某些自身免疫性疾病中具有有害作用。

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How NKG2D ligands trigger autoimmunity?NKG2D配体如何引发自身免疫?
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Tumor-derived NKG2D ligand sMIC reprograms NK cells to an inflammatory phenotype through CBM signalosome activation.
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