Hill H R, Augustine N H, Jaffe H S
Department of Pathology, University of Utah School of Medicine, Salt Lake City 84132.
J Exp Med. 1991 Mar 1;173(3):767-70. doi: 10.1084/jem.173.3.767.
In previous studies, we have reported that after chemotactic factor stimulation, PMNs from neonates fail to undergo certain critical activation steps. Furthermore, the concentration of free intracellular calcium reached is significantly below that of PMNs from adults. Interferon-gamma (IFN-gamma) is a lymphokine that has been shown to activate phagocytic cells, and IFN-gamma messenger RNA production by neonatal mononuclear leukocytes has been reported to be depressed. In the present studies, we found that recombinant human IFN-gamma markedly enhanced the chemotactic responses of PMNs from neonates to levels that were not different from that of PMNs from adults. Furthermore, preincubation of the neonatal cells with this recombinant human lymphokine also corrected the abnormality in intracellular calcium metabolism. These results suggest that this developmental defect in phagocytic cell movement may be the result of an intrinsic defect in IFN-gamma production resulting in deficiency of this critical phagocyte-activating lymphokine.
在先前的研究中，我们已经报道过，在趋化因子刺激后，新生儿的多形核中性粒细胞（PMN）无法经历某些关键的激活步骤。此外，所达到的细胞内游离钙浓度显著低于成人的PMN。γ-干扰素（IFN-γ）是一种已被证明可激活吞噬细胞的淋巴因子，并且据报道新生儿单核白细胞产生的IFN-γ信使核糖核酸水平降低。在本研究中，我们发现重组人IFN-γ显著增强了新生儿PMN的趋化反应，使其达到与成人PMN无异的水平。此外，用这种重组人淋巴因子对新生儿细胞进行预孵育也纠正了细胞内钙代谢的异常。这些结果表明，吞噬细胞运动中的这种发育缺陷可能是由于IFN-γ产生的内在缺陷导致这种关键的吞噬细胞激活淋巴因子缺乏所致。
