Dallegri F, Patrone F, Ballestrero A, Frumento G, Sacchetti C
Clin Exp Immunol. 1984 Sep;57(3):717-21.
The chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine (FMLP), per se incapable of triggering cytotoxicity, was found to significantly enhance phorbol myristate acetate (PMA)-dependent monocyte-mediated cytolysis of human red blood cell (HRBC) targets. Target cell lysis by PMA triggered monocytes was related to the release of superoxide anion and hydrogen peroxide, since cells from patients with chronic granulomatous disease and cells from normal donors, in the presence of superoxide dismutase or catalase, failed to exert significant cytotoxicity. An increased release of these mediators was found to be responsible for the FMLP-dependent amplification of the cytolytic reaction. The results indicate that chemotactic factors are able to enhance the release of cytotoxic mediators by monocytes and raise the possibility that cellular processes during monocyte chemotaxis could modulate the subsequent cytolytic activity.
趋化肽N-甲酰甲硫氨酰-亮氨酰-苯丙氨酸（FMLP）本身不能触发细胞毒性，但被发现能显著增强佛波酯（PMA）依赖的单核细胞介导的对人红细胞（HRBC）靶标的细胞溶解作用。PMA触发的单核细胞对靶细胞的裂解与超氧阴离子和过氧化氢的释放有关，因为慢性肉芽肿病患者的细胞以及正常供体的细胞，在超氧化物歧化酶或过氧化氢酶存在的情况下，无法发挥显著的细胞毒性。发现这些介质释放的增加是FMLP依赖的细胞溶解反应放大的原因。结果表明，趋化因子能够增强单核细胞释放细胞毒性介质，并增加了单核细胞趋化过程中的细胞过程可能调节随后细胞溶解活性的可能性。
