O'Flaherty J T, Rossi A G, Redman J F, Jacobson D P
Department of Medicine, Wake Forest University Medical School, Winston-Salem, NC 27106.
J Immunol. 1991 Dec 1;147(11):3842-7.
TNF-alpha enhances polymorphonuclear responses to many stimuli, including chemotactic peptide FMLP. It also promotes expression of FMLP receptors and thus may prime polymorphonuclear neutrophils to this and other agonists by up-regulating signal recognition molecules. However, we find that the cytokine's actions on FMLP receptors lagged priming of FMLP-induced degranulation. Moreover, TNF-alpha enhanced degranulation responses to leukotriene B4 and platelet-activating factor but paradoxically down-regulated leukotriene B4 receptors and only transiently up-regulated platelet-activating factor receptors. Hence, TNF-alpha has pleiotropic effects on receptor expression; these effects diverge from priming; and a large part of the primed state must reflect enhancement of post-receptor events.
肿瘤坏死因子-α增强多形核细胞对多种刺激的反应，包括趋化肽FMLP。它还促进FMLP受体的表达，因此可能通过上调信号识别分子使多形核中性粒细胞对这种及其他激动剂产生预刺激。然而，我们发现细胞因子对FMLP受体的作用滞后于FMLP诱导的脱颗粒的预刺激。此外，肿瘤坏死因子-α增强了对白三烯B4和血小板活化因子的脱颗粒反应，但自相矛盾的是，它下调了白三烯B4受体，并且只是短暂地上调了血小板活化因子受体。因此，肿瘤坏死因子-α对受体表达具有多效性作用；这些作用与预刺激不同；并且预刺激状态的很大一部分必须反映受体后事件的增强。
