Barber Melissa A, Zhang Tong, Gagne Bethany A, Sentman Charles L
Department of Microbiology and Immunology, Dartmouth Medical School, Lebanon, NH 03756, USA.
J Immunol. 2007 May 15;178(10):6140-7. doi: 10.4049/jimmunol.178.10.6140.
NK cells are known to kill tumor cells and produce proinflammatory cytokines that lead to the generation of tumor-specific CTLs. Many studies have used MHC class I-deficient tumor cells and/or adjuvants that induce NK cell responses. In this study, the focus was on less-immunogenic lymphoma cells that express MHC class I as a model to study NK cell responses to tumors that do not directly stimulate NK cell activation. When RMA tumor cells that expressed a truncated version of OVA, or RMA cells alone, were injected into mice that were depleted of NK cells, the mice developed an increased number of tumor-specific CTLs, increased IFN-gamma responses, and a higher amount of Ag presentation in draining LNs compared with mice with intact NK cells. These data suggest that NK cells can inhibit the development of effective adaptive immunity in the absence of signals that trigger NK cell activation.
已知自然杀伤细胞（NK细胞）可杀伤肿瘤细胞并产生促炎细胞因子，这些细胞因子会导致肿瘤特异性细胞毒性T淋巴细胞（CTL）的产生。许多研究使用了缺乏MHC I类分子的肿瘤细胞和/或诱导NK细胞反应的佐剂。在本研究中，重点是将表达MHC I类分子的免疫原性较低的淋巴瘤细胞作为模型，以研究NK细胞对不直接刺激NK细胞活化的肿瘤的反应。当将表达截短形式OVA的RMA肿瘤细胞或单独的RMA细胞注射到NK细胞耗竭的小鼠体内时，与NK细胞完整的小鼠相比，这些小鼠产生的肿瘤特异性CTL数量增加、γ干扰素反应增强，引流淋巴结中的抗原呈递量也更高。这些数据表明，在缺乏触发NK细胞活化的信号时，NK细胞可抑制有效适应性免疫的发展。
