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机构地区:[1]天津科技大学食品工程与生物技术学院,天津300457
出 处:《现代肿瘤医学》2010年第1期171-176,共6页Journal of Modern Oncology
基 金:国家自然科学基金资助项目(项目编号:20776113);天津科技大学引进人才科研启动基金项目(项目编号:20080426)
摘 要:活化性受体NKG2D(natural-killer group2,member D)和其配基在NK、γδ+T和CD8+T细胞介导的肿瘤免疫应答中扮演了重要角色。NKG2D识别肿瘤细胞表面的配体激活效应细胞,产生有效的抗肿瘤免疫应答。但是在完全具有免疫能力的机体内,表达NKG2D配基的肿瘤仍能够生长发育,因此,在患肿瘤小鼠和肿瘤病人中一定存在着依赖NKG2D的免疫逃避机制。本文就依赖于NKG2D的免疫逃避作一详细综述,主要包括:干涉NKG2D受体的免疫逃避、干涉NKG2D配基的免疫逃避、细胞因子破坏NKG2D受体和配基的免疫逃避、抑制性细胞参与NKG2D介导的免疫逃避。这些研究为抗肿瘤治疗提供了新的途径。The activating receptor NKG2D ( natural - killer group 2, member D) and its ligands play an important role in the NK,γδ^+ and CD8^+ T- cell- mediated immune response to tumors. Engagement of NKG2D ligands on tumor cells by NKG2D triggers effeetor cells to eliminate tumor cells. However, tumors expressing NKG2D ligands can develop in fully immune -competent animals. Therefore, there must exist immune escape mechanisms in tumor mice and cancer patients. This review will provide a broad overview of knowledge of the NKG2D - dependent immune escape, mainly including: immune escape by interference with the NKG2D receptor, immune escape by interference with NKG2D ligands, eytokines impairing the function of NKG2D receptor and NKG2D ligands, suppressor cells involving in NKG2D - mediated immune escape. Recent studies will be a promising strategy for antitumor immune therapy.
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