非刺激性肽在免疫突触处促进抗原诱导的CD8-T细胞受体相互作用。
Nonstimulatory peptides contribute to antigen-induced CD8-T cell receptor interaction at the immunological synapse.
作者信息
Yachi Pia P, Ampudia Jeanette, Gascoigne Nicholas R J, Zal Tomasz
机构信息
Department of Immunology, IMM1, The Scripps Research Institute, La Jolla, California 92037, USA.
出版信息
Nat Immunol. 2005 Aug;6(8):785-92. doi: 10.1038/ni1220. Epub 2005 Jun 26.
Abstract
It is unclear if the interaction between CD8 and the T cell receptor (TCR)-CD3 complex is constitutive or antigen induced. Here, fluorescence resonance energy transfer microscopy between fluorescent chimeras of CD3zeta and CD8beta showed that this interaction was induced by antigen recognition in the immunological synapse. Nonstimulatory endogenous or exogenous peptides presented simultaneously with antigenic peptides increased the CD8-TCR interaction. This finding indicates that the interaction between the intracellular regions of a TCR-CD3 complex recognizing its cognate peptide-major histocompatibility complex (MHC) antigen, and CD8 (plus the kinase Lck), is enhanced by a noncognate CD8-MHC interaction. Thus, the interaction of CD8 with a nonstimulatory peptide-MHC complex helps mediate T cell recognition of antigen, improving the coreceptor function of CD8.
摘要
目前尚不清楚CD8与T细胞受体（TCR）-CD3复合物之间的相互作用是组成性的还是抗原诱导的。在这里，CD3ζ和CD8β荧光嵌合体之间的荧光共振能量转移显微镜显示，这种相互作用是由免疫突触中的抗原识别诱导的。与抗原肽同时呈现的非刺激性内源性或外源性肽增加了CD8-TCR相互作用。这一发现表明，识别其同源肽-主要组织相容性复合体（MHC）抗原的TCR-CD3复合物的细胞内区域与CD8（加上激酶Lck）之间的相互作用通过非同源CD8-MHC相互作用而增强。因此，CD8与非刺激性肽-MHC复合物的相互作用有助于介导T细胞对抗原的识别，改善CD8的共受体功能。
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