CTLs target Th cells that acquire bystander MHC class I-peptide complex from APCs

被引:21
作者
Cox, Jennifer H. [1 ]
McMichael, Andrew J. [1 ]
Screaton, Gavin R. [1 ]
Xu, Xiao-Ning [1 ]
机构
[1] Univ Oxford, John Radcliffe Hosp, Weatherall Inst Mol Med, MRC Human Immunol Unit, Oxford OX3 9DU, England
基金
英国医学研究理事会;
关键词
D O I
10.4049/jimmunol.179.2.830
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
CTLs can acquire MHC class I-peptide complexes from their target cells, whereas CD4(+) T cells obtain MHC class II-peptide complexes from APCs in a TCR-specitic manner. As a consequence, Ag-specific CTL can kill each other (fratricide) or CD4(+) T cells become APCs themselves. The purpose of the acquisition is not fully understood and may be either inhibition or prolongation of an immunological response. In this study, we demonstrate that human CD4(+) Th cells are able to capture membrane fragments from APC during the process of immunological synapse. formation. The fragments contain not only MHC class H-peptide complexes but also MHC class I-peptide complexes, rendering these cells susceptible to CTL killing in an Ag-specilic manner. The control of CD4(+) Th cells by Ag-specific CTL, therefore, maybe another mechanism to regulate CD4(+) T cell expansion in normal immune responses or cause immunopathoglogy during the course of viral infections such as HIV.
引用
收藏
页码:830 / 836
页数:7
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