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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >Human eosinophils produce the T cell-attracting chemokines MIG and IP-10 upon stimulation with IFN-gamma.
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Human eosinophils produce the T cell-attracting chemokines MIG and IP-10 upon stimulation with IFN-gamma.

机译：人嗜酸性粒细胞经IFN-γ刺激后产生吸引T细胞的趋化因子MIG和IP-10。

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摘要

Eosinophils participate in allergic inflammation, where expression of T helper cell type 2 (Th2) cytokines such as interleukin (IL)-4 and IL-5 are seen. However, eosinophils sometimes accumulate during disease with expression of Th1 cytokines [i.e., interferon-gamma (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), and IL-1beta]. In this study, we investigated whether eosinophils can respond with expression of the IFN-inducible C-X-C chemokines monokine induced by IFN-gamma [MIG; CXC chemokine ligand 9 (CXCL9)], IFN-gamma-inducible protein (IP-10/CXCL10), and IFN-inducible T cell alpha chemoattractant (I-TAC/CXCL11). These chemokines share the ability to recruit and activate T cells and natural killer cells to sites of inflammation. We found that IFN-gamma induced rapid and sustained gene expression of MIG, IP-10, and I-TAC in eosinophils, as detected by quantitative reverse transcriptase-polymerase chain reaction. During incubation, IFN-gamma-stimulated eosinophils released MIG and IP-10, as detected by enzyme-linked immunosorbent assay, while I-TAC could not be detected in the medium. TNF-alpha but not IL-1beta enhanced the IFN-gamma-induced production of MIG and IP-10. Conversely, addition of the Th2 cytokine IL-4 down-regulated IFN-gamma-induced synthesis of MIG and IP-10 in eosinophils. Crohn's disease is characterized by a Th1-polarized inflammation and presence of eosinophils. In lesions from this disease, MIG was detected in eosinophils by immunohistochemistry. Taken together, the results point to immunoregulatory roles for eosinophils during some diseases with Th1-polarized inflammation.
机译：嗜酸性粒细胞参与过敏性炎症，在那里可以看到T辅助细胞2型（Th2）细胞因子如白介素（IL）-4和IL-5的表达。然而，嗜酸性粒细胞有时在疾病期间随着Th1细胞因子[即干扰素-γ（IFN-γ），肿瘤坏死因子α（TNF-α）和IL-1β]的表达而积累。在这项研究中，我们调查了嗜酸性粒细胞是否可以响应由IFN-γ诱导的IFN诱导的C-X-C趋化因子单因子的表达[MIG; CXC趋化因子配体9（CXCL9）]，IFN-γ诱导蛋白（IP-10 / CXCL10）和IFN诱导性T细胞α化学引诱剂（I-TAC / CXCL11）。这些趋化因子具有将T细胞和自然杀伤细胞募集并激活至炎症部位的能力。我们发现，通过定量逆转录酶-聚合酶链反应可以检测到，IFN-γ可以诱导嗜酸性粒细胞中MIG，IP-10和I-TAC的快速持续表达。在孵育过程中，通过酶联免疫吸附法检测到，IFN-γ刺激的嗜酸性粒细胞释放了MIG和IP-10，而在培养基中未检测到I-TAC。 TNF-α而非IL-1β增强了IFN-γ诱导的MIG和IP-10的产生。相反，在嗜酸性粒细胞中，Th2细胞因子IL-4的添加下调了IFN-γ诱导的MIG和IP-10的合成。克罗恩病的特征是Th1极化炎症和嗜酸性粒细胞的存在。在该疾病的病变中，通过免疫组织化学在嗜酸性粒细胞中检测到了MIG。两者合计，结果表明嗜酸性粒细胞在某些具有Th1极化炎症的疾病中的免疫调节作用。

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