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首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >Altered collagen II peptides inhibited T-cell activation in rheumatoid arthritis.
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Altered collagen II peptides inhibited T-cell activation in rheumatoid arthritis.

机译：改变的胶原蛋白II肽抑制类风湿关节炎中的T细胞活化。

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摘要

It has been reported that collagen II (CII)-derived peptide induced T-cell activation via its amino acids responsible for T-cell receptor (TCR) recognition. In this study, three altered CII263-272 peptide ligands (APL) containing multiple substitutions of TCR contact residues were synthesized. Their roles in inhibition of T-cell activation were evaluated in peripheral blood lymphocytes (PBL) of rheumatoid arthritis (RA) in vitro. It was shown that 41% (25/61) of RA patients were responsive to the wild-type antigenic CII263-272. In contrast, marginal or silent T-cell responses to the three APLs were found, accompanied by inhibitory effects on secretion of Th1 type cytokines and expression of cell surface markers, CD69 and CD25. In addition, T-cell activation induced by the wild-type antigenic CII263-272 was inhibited by all the three APLs in a dose-dependent manner. It is demonstrated that APLs with substitutions of TCR contact residues are capable of down-regulating T-cell responses in PBLs of RA, suggesting that the CII-derived APLs are potentially therapeutic in RA.
机译：据报道，胶原II（CII）衍生肽通过负责T细胞受体（TCR）识别的氨基酸诱导T细胞活化。在这项研究中，合成了三个具有多个TCR接触残基取代基的CII263-272肽配体（APL）。在类风湿关节炎（RA）的外周血淋巴细胞（PBL）中评估了它们在抑制T细胞活化中的作用。结果表明，RA患者中有41％（25/61）对野生型抗原CII263-272有反应。相反，发现对三种APL的边缘或沉默T细胞应答，伴随有对Th1型细胞因子的分泌和细胞表面标志物CD69和CD25表达的抑制作用。另外，由野生型抗原性CII263-272诱导的T细胞活化被所有三种APL以剂量依赖性方式抑制。已经证明，用TCR接触残基取代的APL能够下调RA的PBL中的T细胞应答，这表明CII衍生的APL可能在RA中具有治疗作用。

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