Chiappelli F, Yamashita N, Faisal M, Kemeny M, Bullington R, Nguyen L, Clement L T, Fahey J L
Psychoneuroimmunology Program, University of California, Los Angeles 90024.
Int J Immunopharmacol. 1991;13(2-3):291-7. doi: 10.1016/0192-0561(91)90110-s.
We have examined in vitro the effect of the proopiomelanocortin gene product, beta-endorphin (bE), on the cytotoxic activity of natural killer (NK) cells, lymphokine activated killer (LAK) cells and cytotoxic T-lymphocytes (CTL). Our studies show that bE reproducibly suppressed LAK cytotoxic activity in all donors tested. The effect of bE on the generation of CTL varied, and was negligible on CTL cytotoxic function. Our study also confirms the variable nature of the effects of bE on NK cytotoxicity. In all instances, the effects of bE were generally small, but could be blocked by opioid receptor antagonists, or by prior heat-inactivation of the peptide. The magnitude of the effects was greatest at low effector:target ratios in all of the three systems studied. These results support the emerging body of evidence that the neuroendocrine system may influence host defense mechanisms mediated by cytotoxic cells.
我们已经在体外研究了阿片促黑皮质素原基因产物β-内啡肽（bE）对自然杀伤（NK）细胞、淋巴因子激活的杀伤（LAK）细胞和细胞毒性T淋巴细胞（CTL）细胞毒性活性的影响。我们的研究表明，bE在所有测试供体中均能重复性地抑制LAK细胞毒性活性。bE对CTL生成的影响各不相同，对CTL细胞毒性功能的影响可忽略不计。我们的研究还证实了bE对NK细胞毒性作用的可变性质。在所有情况下，bE的作用通常较小，但可被阿片受体拮抗剂或肽的预先热灭活所阻断。在所研究的所有三个系统中，效应细胞与靶细胞比例较低时，作用幅度最大。这些结果支持了越来越多的证据，即神经内分泌系统可能影响由细胞毒性细胞介导的宿主防御机制。
