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作 者:S Hussain I Abidi Tao Dong Mai T Vuong Vattipally B Sreenu Sarah L Rowland-Jones Edward J Evans Simon J Davis
机构地区:[1]Nuffield Department of Clinical Medicine and MRC Human Immunology Unit, Weatherall Institute of Molecular Medicine, TheUniversity of Oxford, John Radcliffe Hospital, Headington, Oxford OX3 9DS, UK [2]Present address: Department of Cell Biology,Harvard Medical School, 240 Longwood Avenue, Boston, MA 02115, USA
出 处:《Cell Research》2008年第6期641-648,共8页细胞研究(英文版)
摘 要:CD8 engagement with class I major histocompatibility antigens greatly enhances T-cell activation, but it is not clear how this is achieved. We address the question of whether or not the antibody-mediated ligation of CD8 alone induces transcriptional remodeling in a T-cell clone, using serial analysis of gene expression. Even though it fails to induce overt phenotypic changes, we find that CD8 ligation profoundly alters transcription in the T-cell clone, at a scale comparable to that induced by antibody-mediated ligation of CD3. The character of the resulting changes is distinct, however, with the net effect of CD8 ligation being substantially inhibitory. We speculate that ligating CD8 induces weak, T-cell receptor (TCR)-mediated inhibitory signals reminiscent of the effects of TCR antagonists. Our results imply that CD8 ligation alone is incapable of activating the T-cell clone because it fails to fully induce NFAT-dependent transcription.
关 键 词:receptor triggering signaling CD8 CORECEPTOR SAGE expression analysis
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