Involvement of the 55- and 75-kDa tumor necrosis factor receptors in the generation of lymphokine-activated killer cell activity and proliferation of natural killer cells.
Involvement of the 55- and 75-kDa tumor necrosis factor receptors in the generation of lymphokine-activated killer cell activity and proliferation of natural killer cells.
复制标题
55-和 75-kDa 肿瘤坏死因子受体参与淋巴因子激活的杀伤细胞活性的产生和自然杀伤细胞的增殖。
DOI：
10.4049/jimmunol.146.9.3045
复制
发表时间：
1991
影响因子：
4.4
通讯作者：
T. Espevik
中科院分区：
文献类型：
--
作者：
B. Naume;R. Shalaby;W. Lesslauer;T. Espevik
在这项研究中，我们研究了55 kDa（p55）和75 kDa（p75）的TNF受体在CD 56 + NK细胞中的表达及其在NK细胞和淋巴因子激活的杀伤细胞功能中的作用。通过使用针对p55和p75 TNF-R的mAb，发现NK细胞在活化时表达p55和p75，并且这两种受体都参与淋巴因子活化的杀伤细胞活性的产生。IL-2刺激的NK细胞的增殖活性被抗TNF-α mAb抑制，表明内源性产生的TNF-α对于NK细胞的最佳增殖是重要的。此外，rTNF-α的加入增加了IL-2诱导的NK细胞增殖。抗p55和p75的mAb抑制IL-2诱导的增殖，表明两种TNF-R都参与介导这种作用。
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.