NKG2D公司
细胞毒性T细胞
生物
T细胞
抗原提呈细胞
自然杀伤性T细胞
抗原呈递
T细胞受体
抗原
白细胞介素2受体
CD8型
主要组织相容性复合体
白细胞介素21
细胞生物学
免疫系统
免疫学
CD28
体外
生物化学
作者
Veronika Groh,Rebecca L. Rhinehart,Julie Randolph‐Habecker,Max S. Topp,Stanley R. Riddell,Thomas A. Spies
摘要
NKG2D is an activating receptor that stimulates innate immune responses by natural killer cells upon engagement by MIC ligands, which are induced by cellular stress. Because NKG2D is also present on most CD8alphabeta T cells, it may modulate antigen-specific T cell responses, depending on whether MIC molecules--distant homologs of major histocompatibility complex (MHC) class I with no function in antigen presentation--are induced on the surface of pathogen-infected cells. We found that infection by cytomegalovirus (CMV) resulted in substantial increases in MIC on cultured fibroblast and endothelial cells and was associated with induced MIC expression in interstitial pneumonia. MIC engagement of NKG2D potently augmented T cell antigen receptor (TCR)-dependent cytolytic and cytokine responses by CMV-specific CD28- CD8alphabeta T cells. This function overcame viral interference with MHC class I antigen presentation. Combined triggering of TCR-CD3 complexes and NKG2D induced interleukin 2 production and T cell proliferation. Thus NKG2D functioned as a costimulatory receptor that can substitute for CD28.
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