Giordano M, Geffner J R, Serebrinsky G P, Palermo M S, Isturiz M A
Sección Inmunología, IIHEMA, Academia Nacional de Medicina, Buenos Aires, Argentina.
Immunol Lett. 1988 Feb;17(2):109-13. doi: 10.1016/0165-2478(88)90077-6.
We have previously shown that immune complexes triggered nonspecific cytotoxicity (NSC) towards nonsensitized target cells and antibody-dependent cellular cytotoxicity (ADCC), two functions mediated through monocyte Fc gamma receptors, employing different lytic mechanisms [Geffner, J. R., et al. (1986) Clin. Exp. Immunol. 67, 646]. In this report, we analyze some of the metabolic requirements involved in the induction of monocyte NSC and ADCC. The results showed NSC to be dependent on: (1) metabolic energy derived from glycolysis, (2) availability of external Ca2+, (3) calmodulin activity, (4) integrity of microtubules, but not the microfilament system, and (5) activation of phospholipase(s) and lipoxygenase. On the other hand, ADCC was not impaired by: (1) inhibition of glycolysis, (2) Ca2+ chelation, (3) disruption of microtubules, or (4) inhibition of calmodulin or lipoxygenase. It is concluded that monocyte NSC and ADCC are regulated by different endogenous signals.
我们先前已经表明,免疫复合物可引发对未致敏靶细胞的非特异性细胞毒性(NSC)以及抗体依赖性细胞毒性(ADCC),这两种功能是通过单核细胞Fcγ受体介导的,采用了不同的裂解机制[杰夫纳,J.R.等人(1986年)《临床与实验免疫学》67卷,646页]。在本报告中,我们分析了诱导单核细胞NSC和ADCC所涉及的一些代谢需求。结果表明,NSC依赖于:(1)糖酵解产生的代谢能量,(2)细胞外Ca2+的可用性,(3)钙调蛋白活性,(4)微管的完整性,而非微丝系统,以及(5)磷脂酶和脂氧合酶的激活。另一方面,ADCC不受以下因素影响:(1)糖酵解抑制,(2)Ca2+螯合,(3)微管破坏,或(4)钙调蛋白或脂氧合酶抑制。结论是,单核细胞NSC和ADCC受不同内源性信号调控。