9.1C3分子对人NK细胞和T细胞细胞毒作用的抑制效应

来源 :细胞与分子免疫学杂志 | 被引量 : 0次 | 上传用户:juliediar
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目的探讨9.1C3分子是否作为抑制型受体调节NK细胞和T细胞的杀伤功能。方法用抗CD56抗体和羊抗鼠IgG免疫磁珠分离混合淋巴细胞培养中活化的淋巴细胞 ,分选CD56 +细胞和CD56 -细胞分别作为效应细胞。采用重导向杀伤实验(redirectedkillingassay,RKA)观察抗9.1C3抗体对效应细胞杀伤小鼠肥大细胞瘤细胞P815作用的影响。结果发现人NK细胞和T细胞对P815细胞均有一定的杀伤作用 ,在效靶比为4∶1 ,2∶1和1∶1时 ,NK细胞和T细胞的杀伤率分别为:6.4% ,3.4% ,1.1%和21.2 % ,16.7 % ,6.5 %。用抗CD16和抗CD3抗体分别刺激NK细胞和T细胞时 ,它们对P815细胞的细胞毒作用显著增强 ;在相同的效靶比例 ,它们对P815的杀伤率分别为:47.1 % ,32.2% ,19.1 %和64.4 % ,50.3% ,39.5 %。但用抗9.1C3抗体刺激效应细胞时 ,不仅NK细胞的杀伤作用完全被抑制 ,CD16介导的NK细胞的杀伤作用也被明显下调 ,其杀伤率仅为18.5 % ,9.7 %和7.0 % ;但对CD3介导的T细胞的杀伤作用只轻度被抑制。结论9.1C3分子可能是一种新的抑制型杀伤细胞受体 ,对NK细胞和T细胞细胞毒作用的负调节可能有所不同。 Objective To investigate whether 9.1C3 regulates NK cell and T cell killing function as an inhibitory receptor. Methods The activated lymphocytes in mixed lymphocyte culture were isolated by anti-CD56 and goat anti-mouse IgG immunomagnetic beads. CD56 + cells and CD56 - cells were sorted as effector cells. The effect of anti-9.1C3 antibody on the effect of P815 in mast cell of mice was studied by redirected killing assay (RKA). The results showed that human NK cells and T cells had a certain killing effect on P815 cells. The killing rates of NK cells and T cells at the target ratios of 4: 1, 2: 1 and 1: 1 were 6.4% 3.4%, 1.1% and 21.2%, 16.7% and 6.5% respectively. When NK cells and T cells were stimulated with anti-CD16 and anti-CD3 antibodies respectively, their cytotoxic effects on P815 cells were significantly enhanced. The killing rates of P815 at the same target ratio were 47.1%, 32.2%, 19.1 % And 64.4%, 50.3%, 39.5%. However, when anti-9.1C3 antibody was used to stimulate effector cells, not only the killing effect of NK cells was completely inhibited, but also the killing effect of CD16-mediated NK cells was significantly down-regulated, killing rate was only 18.5%, 9.7% and 7.0% The killing effect on CD3-mediated T cells is only modestly inhibited. Conclusion 9.1C3 may be a new inhibitor of killer cell receptors, and may negatively regulate the cytotoxicity of NK cells and T cells.
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