Bauer S, Groh V, Wu J, Steinle A, Phillips J H, Lanier L L, Spies T
Fred Hutchinson Cancer Research Center, Clinical Research Division, 1100 Fairview Avenue North, Seattle, WA 98109, USA.
Science. 1999 Jul 30;285(5428):727-9. doi: 10.1126/science.285.5428.727.
Stress-inducible MICA, a distant homolog of major histocompatibility complex (MHC) class I, functions as an antigen for gammadelta T cells and is frequently expressed in epithelial tumors. A receptor for MICA was detected on most gammadelta T cells, CD8+ alphabeta T cells, and natural killer (NK) cells and was identified as NKG2D. Effector cells from all these subsets could be stimulated by ligation of NKG2D. Engagement of NKG2D activated cytolytic responses of gammadelta T cells and NK cells against transfectants and epithelial tumor cells expressing MICA. These results define an activating immunoreceptor-MHC ligand interaction that may promote antitumor NK and T cell responses.
应激诱导的MICA是主要组织相容性复合体（MHC）I类的远亲同源物，作为γδT细胞的抗原，且在上皮肿瘤中经常表达。在大多数γδT细胞、CD8⁺αβT细胞和自然杀伤（NK）细胞上检测到MICA的一种受体，并将其鉴定为NKG2D。所有这些亚群的效应细胞都可通过NKG2D的连接而被刺激。NKG2D的结合激活了γδT细胞和NK细胞对表达MICA的转染细胞和上皮肿瘤细胞的溶细胞反应。这些结果定义了一种可能促进抗肿瘤NK和T细胞反应的激活免疫受体-MHC配体相互作用。
