Naume B, Shalaby R, Lesslauer W, Espevik T
Institute of Cancer Research, University of Trondheim, Norway.
J Immunol. 1991 May 1;146(9):3045-8.
In this study we investigated the expression of the 55 kDa (p55) and the 75 kDa (p75) TNF receptors in CD56+ NK cells and their role in NK and lymphokine-activated killer cells cell functions. By using mAb against the p55 and p75 TNF-R, NK cells were found to express both p55 and p75 upon activation, and both receptors were involved in the generation of lymphokine-activated killer cells activity. Proliferative activity of IL-2 stimulated NK cells was inhibited by anti-TNF-alpha mAb, indicating that endogenously produced TNF-alpha is important for optimal proliferation of NK cells. Furthermore, addition of rTNF-alpha increased the IL-2-induced proliferation of NK cells. mAb to p55 and p75 inhibited the IL-2-induced proliferation indicating that both TNF-R are involved in mediating this effect.
在本研究中，我们调查了55 kDa（p55）和75 kDa（p75）肿瘤坏死因子受体在CD56 + 自然杀伤细胞中的表达及其在自然杀伤细胞和淋巴因子激活的杀伤细胞功能中的作用。通过使用抗p55和p75肿瘤坏死因子受体的单克隆抗体，发现自然杀伤细胞在激活后同时表达p55和p75，并且这两种受体都参与了淋巴因子激活的杀伤细胞活性的产生。抗TNF-α单克隆抗体抑制了IL-2刺激的自然杀伤细胞的增殖活性，表明内源性产生的TNF-α对自然杀伤细胞的最佳增殖很重要。此外，添加重组TNF-α增加了IL-2诱导的自然杀伤细胞增殖。抗p55和p75的单克隆抗体抑制了IL-2诱导的增殖，表明这两种肿瘤坏死因子受体都参与介导这种效应。
