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多种肽与MHC I类分子的结合会抑制活化的自然杀伤细胞对靶细胞的裂解。

Binding of diverse peptides to MHC class I molecules inhibits target cell lysis by activated natural killer cells.

作者信息

Correa I, Raulet D H

机构信息

Department of Molecular and Cell Biology, University of California, Berkeley 94720, USA.

出版信息

Immunity. 1995 Jan;2(1):61-71. doi: 10.1016/1074-7613(95)90079-9.

DOI:10.1016/1074-7613(95)90079-9
PMID:7541307
Abstract

Class I MHC expression by target cells inhibits lysis mediated by natural killer (NK) cells, often in an allele-specific fashion. It has been proposed that NK cell inhibitory receptors recognize complexes of class I molecules with specific cellular peptides that define self, displacement of which would render cells NK sensitive. By loading the mostly empty Dd class I molecules of cell lines deficient in peptide transporter molecules with synthetic or natural Dd-bound peptides, we have demonstrated specific dose-dependent inhibition of the Ly49+ subset of activated NK cells by class I-peptide complexes. Inhibition occurred with most if not all Dd-binding peptides, suggesting that Ly49+ NK cells recognize class I-peptide complexes largely independently of peptide composition. The results suggest a primary role of NK cells in the destruction of cells that have down-regulated or extinguished cell surface expression of some or all class I molecules.

摘要

靶细胞上的I类主要组织相容性复合体(MHC)表达通常以等位基因特异性方式抑制自然杀伤(NK)细胞介导的细胞裂解。有人提出,NK细胞抑制性受体识别I类分子与定义自身的特定细胞肽的复合物,这些肽的置换会使细胞对NK敏感。通过用合成或天然的与Dd结合的肽加载缺乏肽转运分子的细胞系中几乎为空的Dd I类分子,我们证明了I类肽复合物对活化NK细胞的Ly49 +亚群具有特异性剂量依赖性抑制作用。大多数(如果不是全部)与Dd结合的肽都能产生抑制作用,这表明Ly49 + NK细胞识别I类肽复合物在很大程度上与肽的组成无关。结果表明,NK细胞在破坏下调或消除部分或全部I类分子细胞表面表达的细胞中起主要作用。

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