Al-Aoukaty A, Rolstad B, Giaid A, Maghazachi A A
Department of Anatomy, University of Oslo, Oslo, Norway.
Immunology. 1998 Dec;95(4):618-24. doi: 10.1046/j.1365-2567.1998.00603.x.
We demonstrate here that the CC chemokines macrophage inflammatory protein-3alpha (MIP-3alpha), macrophage inflammatory protein-3beta (MIP-3beta) and the CX3C chemokine fractalkine induce the chemotaxis of interleukin-2 (IL-2)-activated natural killer (IANK) cells. In addition, these chemokines enhance the binding of [gamma-35S]guanine triphosphate ([gamma-35S]GTP) to IANK cell membranes, suggesting that receptors for these chemokines are G protein-coupled. Our results show that MIP-3alpha receptors are coupled to Go, Gq and Gz, MIP-3beta receptors are coupled to Gi, Gq and Gs, whereas fractalkine receptors are coupled to Gi, and Gz. All three chemokines induced a robust calcium response flux in IANK cells. Cross-desensitization experiments show that MIP-3alpha, MIP-3beta or fractalkine use receptors not shared by each other or by the CC chemokine regulated on activation, normal, T-cell expressed, and secreted (RANTES), the CXC chemokines stromal-derived factor-1alpha (SDF-1alpha) and interferon-inducible protein-10 (IP-10), or the C chemokine lymphotactin.
我们在此证明，CC趋化因子巨噬细胞炎性蛋白-3α（MIP-3α）、巨噬细胞炎性蛋白-3β（MIP-3β）以及CX3C趋化因子fractalkine可诱导白细胞介素-2（IL-2）激活的自然杀伤（IANK）细胞的趋化作用。此外，这些趋化因子可增强[γ-35S]鸟嘌呤三磷酸（[γ-35S]GTP）与IANK细胞膜的结合，提示这些趋化因子的受体是G蛋白偶联受体。我们的结果表明，MIP-3α受体与Go、Gq和Gz偶联，MIP-3β受体与Gi、Gq和Gs偶联，而fractalkine受体与Gi和Gz偶联。所有这三种趋化因子均可在IANK细胞中诱导强烈的钙反应通量。交叉脱敏实验表明，MIP-3α、MIP-3β或fractalkine使用的受体彼此之间不共享，也与CC趋化因子（激活调节正常T细胞表达和分泌的趋化因子，RANTES）、CXC趋化因子基质衍生因子-1α（SDF-1α）和干扰素诱导蛋白-10（IP-10）或C趋化因子淋巴细胞趋化素所使用的受体不同。
