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首页> 外文期刊>The journal of immunology >Cutting Edge: Species Specificity of the CC Chemokine 6Ckine Signaling Through the CXC Chemokine Receptor CXCR3: Human 6Ckine Is Not A Ligand for the Human or Mouse CXCR3 Receptors
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Cutting Edge: Species Specificity of the CC Chemokine 6Ckine Signaling Through the CXC Chemokine Receptor CXCR3: Human 6Ckine Is Not A Ligand for the Human or Mouse CXCR3 Receptors

机译:前沿:通过CXC趋化因子受体CXCR3发出CC趋化因子6Ckine信号的物种特异性:人6Ckine不是人或小鼠CXCR3受体的配体

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The CC chemokine known as 6Ckine (SLC, Exodus-2, or TCA4) has been identified as a ligand for CCR7. Mouse 6Ckine has also been shown to signal through mouse CXCR3 and share some of the activities of IFN-γ inducible protein 10 and monokine induced by IFN-γ. Nonetheless, human 6Ckine has not been shown to bind CXCR3 receptor or have angiostatic activity. In this study, we report that human 6Ckine does not induce a calcium flux in either human CXCR3 or mouse CXCR3 transfected cells, although it is an equally potent agonist as mouse 6Ckine and human macrophage inflammatory protein-3β in human CCR7 transfected cells. Mouse 6Ckine (but not human 6Ckine) is capable of competing with radiolabeled IFN-γ inducible protein 10 for human CXCR3. In addition, radiolabeled human 6Ckine does not bind to either human CXCR3 or mouse CXCR3. Together these data suggest that human CC chemokine 6Ckine is not a ligand for the human or mouse CXC chemokine receptor CXCR3.
机译:CC趋化因子称为6Ckine(SLC,Exodus-2或TCA4)已被鉴定为CCR7的配体。还显示了小鼠6Ckine通过小鼠CXCR3发出信号,并具有IFN-γ诱导蛋白10和IFN-γ诱导的单因子的某些活性。但是,尚未显示人6Ckine结合CXCR3受体或具有血管抑制活性。在这项研究中,我们报道了人6Ckine在人CXCR3或小鼠CXCR3转染的细胞中均不会诱导钙通量,尽管它在人CCR7转染的细胞中与小鼠6Ckine和人巨噬细胞炎性蛋白3β具有同等效力。小鼠6Ckine(而非人6Ckine)能够与放射性标记的IFN-γ诱导蛋白10竞争人CXCR3。另外,放射性标记的人6Ckine不与人CXCR3或小鼠CXCR3结合。这些数据共同表明,人CC趋化因子6Ckine不是人或小鼠CXC趋化因子受体CXCR3的配体。

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