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Identification of an alternative G{alpha}q-dependent chemokine receptor signal transduction pathway in dendritic cells and granulocytes

机译:树突状细胞和粒细胞中另一种依赖G {alpha} q的趋化因子受体信号转导途径的鉴定

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摘要

CD38 controls the chemotaxis of leukocytes to some, but not all, chemokines, suggesting that chemokine receptor signaling in leukocytes is more diverse than previously appreciated. To determine the basis for this signaling heterogeneity, we examined the chemokine receptors that signal in a CD38-dependent manner and identified a novel "alternative" chemokine receptor signaling pathway. Similar to the "classical" signaling pathway, the alternative chemokine receptor pathway is activated by G{alpha}i2-containing Gi proteins. However, unlike the classical pathway, the alternative pathway is also dependent on the Gq class of G proteins. We show that G{alpha}q-deficient neutrophils and dendritic cells (DCs) make defective calcium and chemotactic responses upon stimulation with N-formyl methionyl leucyl phenylalanine and CC chemokine ligand (CCL) 3 (neutrophils), or upon stimulation with CCL2, CCL19, CCL21, and CXC chemokine ligand (CXCL) 12 (DCs). In contrast, G{alpha}q-deficient T cell responses to CXCL12 and CCL19 remain intact. Thus, the alternative chemokine receptor pathway controls the migration of only a subset of cells. Regardless, the novel alternative chemokine receptor signaling pathway appears to be critically important for the initiation of inflammatory responses, as G{alpha}q is required for the migration of DCs from the skin to draining lymph nodes after fluorescein isothiocyanate sensitization and the emigration of monocytes from the bone marrow into inflamed skin after contact sensitization.
机译:CD38控制白细胞对某些但不是全部趋化因子的趋化性,这表明白细胞中趋化因子受体的信号传导比以前所认识的更加多样化。为了确定这种信号异质性的基础,我们检查了以CD38依赖性方式发信号的趋化因子受体,并鉴定了新的“替代”趋化因子受体信号通路。类似于“经典的”信号传导途径,替代的趋化因子受体途径被含Gα12的Gi蛋白激活。但是,不同于经典途径,替代途径也依赖于Gq类G蛋白。我们显示,G {alpha} q缺乏中性粒细胞和树突状细胞(DC)在受到N-甲酰基甲硫基亮氨酰苯丙氨酸和CC趋化因子配体(CCL)3(中性粒细胞)刺激后,或由CCL2刺激后,会产生有缺陷的钙和趋化反应, CCL19,CCL21和CXC趋化因子配体(CXCL)12(DC)。相反,对CXCL12和CCL19的Gαq缺乏的T细胞应答保持完整。因此,替代的趋化因子受体途径控制仅细胞子集的迁移。无论如何,新颖的替代趋化因子受体信号转导途径对于炎症反应的启动似乎至关重要,因为在荧光素异硫氰酸酯敏化和单核细胞迁移后,从皮肤向排水淋巴结的DC迁移需要G {q} q接触致敏后从骨髓进入发炎的皮肤。

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