van den Broek M F, Kägi D, Zinkernagel R M, Hengartner H
Institute of Experimental Immunology, University of Zürich, Switzerland.
Eur J Immunol. 1995 Dec;25(12):3514-6. doi: 10.1002/eji.1830251246.
Adaptive immune surveillance by T cells against infections and tumors depends on the presence of antigenic peptides presented by major histocompatibility complex (MHC) molecules. If antigenic tumor-specific peptides or MHC class I molecules are absent, the adaptive T cell immune response fails. Natural killer (NK) cells seem to complement the specific T cells by recognizing target cells lacking MHC class I (e.g. RMA-S). The role of perforin, which is crucially involved in T cell and NK cell-mediated target cell lysis, was evaluated in mice lacking perforin with respect to their capacity to eliminate a syngeneic lymphoid tumor. Here, we show that growth of MHC class I RMA-S tumor cells in unprimed mice was controlled by NK cells through perforin-dependent cytotoxicity.
T细胞针对感染和肿瘤的适应性免疫监视依赖于主要组织相容性复合体(MHC)分子所呈递的抗原肽的存在。如果缺乏抗原性肿瘤特异性肽或MHC I类分子,适应性T细胞免疫反应就会失败。自然杀伤(NK)细胞似乎通过识别缺乏MHC I类分子的靶细胞(如RMA-S细胞)来补充特异性T细胞。穿孔素在T细胞和NK细胞介导的靶细胞裂解中起关键作用,本研究在缺乏穿孔素的小鼠中评估了其清除同基因淋巴瘤的能力。在此,我们表明,未致敏小鼠体内MHC I类RMA-S肿瘤细胞通过NK细胞的穿孔素依赖性细胞毒性得到控制。