Tsou C L, Gladue R P, Carroll L A, Paradis T, Boyd J G, Nelson R T, Neote K, Charo I F
Gladstone Institute of Cardiovascular Disease, the Cardiovascular Research Institute, and the Department of Medicine, University of California, San Francisco, California 94141, USA.
J Exp Med. 1998 Aug 3;188(3):603-8. doi: 10.1084/jem.188.3.603.
Hemofiltrate C-C chemokine (HCC)-1 is a recently cloned C-C chemokine that is structurally similar to macrophage inflammatory protein (MIP)-1alpha. Unlike most chemokines, it is constitutively secreted by tissues and is present at high concentrations in normal human plasma. Also atypical for chemokines, HCC-1 is reported not to be chemotactic for leukocytes. In this paper, we have investigated the chemokine receptor usage and downstream signaling pathways of HCC-1. Cross-desensitization experiments using THP-1 cells suggested that HCC-1 and MIP-1alpha activated the same receptor. Experiments using a panel of cloned chemokine receptors revealed that HCC-1 specifically activated C-C chemokine receptor (CCR)1, but not closely related receptors, including CCR5. HCC-1 competed with MIP-1alpha for binding to CCR1-transfected cells, but with a markedly reduced affinity (IC50 = 93 nM versus 1.3 nM for MIP-1alpha). Similarly, HCC-1 was less potent than MIP-1alpha in inducing inhibition of adenylyl cyclase in CCR1-transfected cells. HCC-1 induced chemotaxis of freshly isolated human monocytes, THP-1 cells, and CCR1-transfected cells, and the optimal concentration for cell migration (100 nM) was approximately 100-fold lower than that of MIP-1alpha (1 nM). These data demonstrate that HCC-1 is a chemoattractant and identify CCR1 as a functional HCC-1 receptor on human monocytes.
血液滤过液C-C趋化因子(HCC)-1是最近克隆出的一种C-C趋化因子,其结构与巨噬细胞炎性蛋白(MIP)-1α相似。与大多数趋化因子不同,它由组织组成性分泌,在正常人血浆中浓度较高。HCC-1在趋化因子中也不典型,据报道它对白细胞没有趋化作用。在本文中,我们研究了HCC-1的趋化因子受体用途和下游信号通路。使用THP-1细胞进行的交叉脱敏实验表明,HCC-1和MIP-1α激活相同的受体。使用一组克隆趋化因子受体进行的实验表明,HCC-1特异性激活C-C趋化因子受体(CCR)1,但不激活包括CCR5在内的密切相关受体。HCC-1与MIP-1α竞争结合CCR1转染细胞,但亲和力明显降低(IC50 = 93 nM,而MIP-1α为1.3 nM)。同样,在诱导CCR1转染细胞中腺苷酸环化酶抑制方面,HCC-1的效力低于MIP-1α。HCC-1诱导新鲜分离的人单核细胞、THP-1细胞和CCR1转染细胞的趋化作用,细胞迁移的最佳浓度(100 nM)比MIP-1α(1 nM)低约100倍。这些数据表明HCC-1是一种趋化因子,并确定CCR1是人类单核细胞上功能性的HCC-1受体。