Gene expression and production of the monokine induced by IFN-gamma (MIG), IFN-inducible T cell alpha chemoattractant (I-TAC), and IFN-gamma-inducible protein-10 (IP-10) chemokines by human neutrophils.
Gene expression and production of the monokine induced by IFN-gamma (MIG), IFN-inducible T cell alpha chemoattractant (I-TAC), and IFN-gamma-inducible protein-10 (IP-10) chemokines by human neutrophils.
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发表时间：
1999-04
影响因子：
4.4
通讯作者：
S. Gasperini;M. Marchi;F. Calzetti;Carlo Laudanna;L. Vicentini;Henrik S. Olsen;Marianne Murphy;Fang Liao;Joshua M. Farber;M. Cassatella
中科院分区：
文献类型：
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作者：
S. Gasperini;M. Marchi;F. Calzetti;Carlo Laudanna;L. Vicentini;Henrik S. Olsen;Marianne Murphy;Fang Liao;Joshua M. Farber;M. Cassatella
由IFN-γ诱导的单核因子（IFN-γ）、IFN-诱导的T细胞α化学引诱物（I-TAC）和IFN-γ诱导的10 kDa蛋白（IP-10）是CXC趋化因子亚家族的相关成员，其结合共同受体CXCR 3，并且由不同细胞类型响应IFN-γ产生。我们最近报道，人类多形核中性粒细胞（PMN）有能力释放IP-10。在此，我们表明，中性粒细胞也有能力产生IFN-γ和表达I-TAC mRNA的组合与TNF-α或LPS。IFN-γ单独或与激动剂如fMLP、IL-8、粒细胞（G）-CSF和粒细胞-巨噬细胞（GM）-CSF联合不能影响IFN-γ、IP-10和I-TAC基因表达，而IFN-α与TNF-α、LPS或IL-1 β联合可显著诱导中性粒细胞释放IP-10。此外，IL-10和IL-4显着抑制IFN-γ加LPS或TNF-α刺激的中性粒细胞中IFN-γ、IP-10和I-TAC mRNA的表达以及IFN-γ和IP-10的细胞外产生。最后，收获的上清液刺激PMN诱导迁移和快速整合素依赖性粘附的CXCR 3表达淋巴细胞，这些活动显着降低了中和的抗CD 4和抗IP-10抗体，这表明它们介导的CD 4和IP-10存在于上清液中。由于IL-10、IP-10和I-TAC是NK细胞和Th 1淋巴细胞的有效趋化因子，因此中性粒细胞产生这些趋化因子的能力可能不仅有助于炎症反应的进展和演变，而且有助于免疫反应的调节。
Monokine induced by IFN-gamma (MIG), IFN-inducible T cell alpha chemoattractant (I-TAC), and IFN-gamma-inducible protein of 10 kDa (IP-10) are related members of the CXC chemokine subfamily that bind to a common receptor, CXCR3, and that are produced by different cell types in response to IFN-gamma. We have recently reported that human polymorphonuclear neutrophils (PMN) have the capacity to release IP-10. Herein, we show that PMN also have the ability to produce MIG and to express I-TAC mRNA in response to IFN-gamma in combination with either TNF-alpha or LPS. While IFN-gamma, alone or in association with agonists such as fMLP, IL-8, granulocyte (G)-CSF and granulocyte-macrophage (GM)-CSF, failed to influence MIG, IP-10, and I-TAC gene expression, IFN-alpha, in combination with TNF-alpha, LPS, or IL-1beta, resulted in a considerable induction of IP-10 release by neutrophils. Furthermore, IL-10 and IL-4 significantly suppressed the expression of MIG, IP-10, and I-TAC mRNA and the extracellular production of MIG and IP-10 in neutrophils stimulated with IFN-gamma plus either LPS or TNF-alpha. Finally, supernatants harvested from stimulated PMN induced migration and rapid integrin-dependent adhesion of CXCR3-expressing lymphocytes; these activities were significantly reduced by neutralizing anti-MIG and anti-IP-10 Abs, suggesting that they were mediated by MIG and IP-10 present in the supernatants. Since MIG, IP-10, and I-TAC are potent chemoattractants for NK cells and Th1 lymphocytes, the ability of neutrophils to produce these chemokines might contribute not only to the progression and evolution of the inflammatory response, but also to the regulation of the immune response.