Peptide antagonism and T cell receptor interactions with peptide-MHC complexes.
Peptide antagonism and T cell receptor interactions with peptide-MHC complexes.
复制标题
肽拮抗作用以及 T 细胞受体与肽-MHC 复合物的相互作用。
DOI：
10.1016/s1074-7613(00)80631-7
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发表时间：
1998
期刊：
影响因子：
32.4
通讯作者：
Eisen,HN
中科院分区：
文献类型：
--
作者：
Sykulev,Y;Vugmeyster,Y;Brunmark,A;Ploegh,HL;Eisen,HN
我们描述了特异性抑制T细胞克隆和表达CD8+T淋巴细胞克隆2C抗原特异性受体的拮抗肽，该受体识别与同基因(KB)和同种(LD)MHC蛋白相关的多肽。加入能与Kbon 2C细胞结合的拮抗肽可降低细胞预先暴露于激动肽Kb复合体所引起的CD3ζ链的酪氨酸磷酸化。与以往激动剂-拮抗剂的比较相反，2C T细胞受体与拮抗肽Kb复合体的亲和力高于与弱激动肽Kb复合体的亲和力。考虑这种差异的依据是，有证据表明，当用活细胞上的受体测定抗原特异性受体亲和力时，比用无细胞系统中的受体测定时要高得多。
We describe antagonist peptides that specifically inhibit cytolytic activity of T cell clones and lines that express the antigen-specific receptor of CD8+T lymphocyte clone 2C, which recognizes peptides in association with syngeneic (Kb) and allogeneic (Ld) MHC proteins. Addition of an antagonist peptide that can bind to Kbon 2C cells decreased the tyrosine phosphorylation of CD3 ζ chains elicited by prior exposure of the cells to an agonist peptide-Kbcomplex. Contrary to previous agonist-antagonist comparisons, the 2C T cell receptor had higher affinity for an antagonist peptide-Kbcomplex than for a weak agonist peptide-Kbcomplex. This difference is considered in light of evidence that antigen-specific receptor affinity values can be substantially higher when determined with the receptor on live cells than with the receptor in cell-free systems.