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外周血T淋巴细胞上主要组织相容性复合体I类分子的结扎诱导新的表型和功能。

Ligation of MHC class I molecules on peripheral blood T lymphocytes induces new phenotypes and functions.

作者信息

Bregenholt S, Röpke M, Skov S, Claesson M H

机构信息

Laboratory of Experimental Immunology, Department of Medical Anatomy, The Panum Institute, University of Copenhagen, Copenhagen, Denmark.

出版信息

J Immunol. 1996 Aug 1;157(3):993-9.

PMID:8757602
Abstract

Microgram concentrations of immobilized anti-MHC class I (MHC-I) Ab induced proliferation of resting CD3+ T cells from peripheral blood. In contrast, soluble Ab did not activate T cells. Exposure of T cells to immobilized anti-MHC-I Ab for only 24 h was followed by proliferation and development of T cell-mediated cytotoxicity. Immediately following MHC-I ligation, the T cells responded with increased protein tyrosine phosphorylation, with new bands appearing in the SDS-PAGE. Exposure of T cells to immobilized anti-MHC-I Ab for 24 h induced an increased surface expression of the TCR/CD3 and CD28 molecules. MHC-I-induced proliferation of purified T cells was dependent on cellular interactions with non-T cells. Under certain conditions, in which MHC-I was ligated by picogram concentrations of immobilized anti-MHC-I Ab, anti-TCR/CD3 Ab-induced proliferation of T cells was strongly inhibited. These data clearly demonstrate that ligation of the MHC-I complex on T cells may induce both positive and negative signals. Since the physiologic ligands for MHC-I molecules are TCR and the CD8 molecules, our data may suggest that MHC-I molecules are instrumental in cellular interactions between T cells.

摘要

微克浓度的固定化抗MHC I类(MHC-I)抗体可诱导外周血中静息CD3⁺ T细胞增殖。相比之下,可溶性抗体不能激活T细胞。T细胞仅暴露于固定化抗MHC-I抗体24小时后,就会出现增殖并发展出T细胞介导的细胞毒性。MHC-I连接后,T细胞立即出现蛋白质酪氨酸磷酸化增加,SDS-PAGE中出现新条带。T细胞暴露于固定化抗MHC-I抗体24小时可诱导TCR/CD3和CD28分子的表面表达增加。MHC-I诱导的纯化T细胞增殖依赖于细胞与非T细胞的相互作用。在某些条件下,当皮克浓度的固定化抗MHC-I抗体连接MHC-I时,抗TCR/CD3抗体诱导的T细胞增殖受到强烈抑制。这些数据清楚地表明,T细胞上MHC-I复合物的连接可能诱导正性和负性信号。由于MHC-I分子的生理配体是TCR和CD8分子,我们的数据可能表明MHC-I分子在T细胞之间的细胞相互作用中起作用。

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