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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >I-TAC/CXCL11 is a natural antagonist for CCR5.
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I-TAC/CXCL11 is a natural antagonist for CCR5.

机译：I-TAC / CXCL11是CCR5的天然拮抗剂。

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摘要

The selective CXC chemokine receptor 3 (CXCR3) agonists, monokine induced by interferon-gamma (IFN- gamma)/CXC chemokine ligand 9 (CXCL9), IFN-inducible protein 10/CXCL10, and IFN-inducible T cell alpha chemoattractant (I-TAC)/CXCL11, attract CXCR3+ cells such as CD45RO+ T lymphocytes, B cells, and natural killer cells. Further, all three chemokines are potent, natural antagonists for chemokine receptor 3 (CCR3) and feature defensin-like, antimicrobial activities. In this study, we show that I-TAC, in addition to these effects, acts as an antagonist for CCR5. I-TAC inhibited the binding of macrophage-inflammatory protein-1alpha (MIP-1alpha)/CC chemokine ligand 3 (CCL3) to cells transfected with CCR5 and to monocytes. Furthermore, cell migration evoked by regulated on activation, normal T expressed and secreted (RANTES)/CCL5 and MIP-1beta/CCL4, the selective agonist of CCR5, was inhibited in transfected cells and monocytes, respectively. In two other functional assays, namely the release of free intracellular calcium and actin polymerization, I-TAC reduced CCR5 activities to minimal levels. Sequence and structure analyses indicate a potential role for K17, K49, and Q51 of I-TAC in CCR5 binding. Our results expand on the potential role of I-TAC as a negative modulator in leukocyte migration and activation, as I-TAC would specifically counteract the responses mediated by many "classical," inflammatory chemokines that act not only via CCR3 but via CCR5 as well.
机译：选择性CXC趋化因子受体3（CXCR3）激动剂，由干扰素-γ（IFN-γ）/ CXC趋化因子配体9（CXCL9），IFN诱导型蛋白10 / CXCL10和IFN诱导的T细胞α趋化因子（I- TAC）/ CXCL11，吸引CXCR3 +细胞，例如CD45RO + T淋巴细胞，B细胞和自然杀伤细胞。此外，所有三种趋化因子都是趋化因子受体3（CCR3）的有效天然拮抗剂，并具有类似防御素的抗菌活性。在这项研究中，我们表明I-TAC除了这些作用外，还可以作为CCR5的拮抗剂。 I-TAC抑制巨噬细胞炎症蛋白1alpha（MIP-1alpha）/ CC趋化因子配体3（CCL3）与转染CCR5的细胞和单核细胞的结合。此外，通过调节激活，正常的T表达和分泌（RANTES）/ CCL5和MIP-1beta / CCL4（CCR5的选择性激动剂）引起的细胞迁移分别在转染的细胞和单核细胞中受到抑制。在另外两个功能测定中，即游离细胞内钙的释放和肌动蛋白聚合，I-TAC将CCR5活性降至最低水平。序列和结构分析表明I-TAC的K17，K49和Q51在CCR5结合中具有潜在作用。我们的结果扩展了I-TAC作为白细胞迁移和激活中的负调节剂的潜在作用，因为I-TAC可以特异性抵消由许多“经典”炎症趋化因子介导的反应，这些趋化因子不仅通过CCR3，而且通过CCR5起作用。 。

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