疱疹病毒8编码的趋化因子vMIP-II可抑制CCR10受体，而痘病毒编码的趋化因子MC148则不能。

The herpesvirus 8-encoded chemokine vMIP-II, but not the poxvirus-encoded chemokine MC148, inhibits the CCR10 receptor.

作者信息

Lüttichau H R, Lewis I C, Gerstoft J, Schwartz T W

机构信息

Laboratory for Molecular Pharmacology, Department of Pharmacology, Panum Institute, Copenhagen, Denmark.

出版信息

Eur J Immunol. 2001 Apr;31(4):1217-20. doi: 10.1002/1521-4141(200104)31:4<1217::aid-immu1217>3.0.co;2-s.

DOI:10.1002/1521-4141(200104)31:4<1217::aid-immu1217>3.0.co;2-s

PMID:11298347

Abstract

The viral chemokine antagonist vMIP-II encoded by human herpesvirus 8 (HHV8) and MC148 encoded by the poxvirus - Molluscum contagiosum - were tested against the newly identified chemokine receptor CCR10. As the CCR10 ligand ESkine / CCL27 had the highest identity to MC148 and because both chemokines are expressed in the skin we suspected MC148 to block CCR10. However, in calcium mobilization assays we found MC148 unable to block CCR10 in micromolar concentrations in contrast to vMIP-II. (125)I-MC148 was only able to bind to CCR8, but not to CCR10, CCR11, CXCR6 / BONZO, APJ, DARC or the orphan receptors BOB, EBI-II, GPR4, GPR17, HCR or RDC1. We conclude that MC148 is a highly selective CCR8 antagonist conceivably optimized to interfere with NK cell and monocyte invasion, whereas the broad-spectrum antagonist vMIP-II protects HHV8 by blocking multiple receptors.

摘要

对由人类疱疹病毒8型（HHV8）编码的病毒趋化因子拮抗剂vMIP-II和由痘病毒——传染性软疣——编码的MC148针对新鉴定出的趋化因子受体CCR10进行了测试。由于CCR10配体ESkine / CCL27与MC148的同源性最高，并且因为这两种趋化因子都在皮肤中表达，我们怀疑MC148会阻断CCR10。然而，在钙动员试验中，我们发现与vMIP-II不同，MC148在微摩尔浓度下无法阻断CCR10。(125)I-MC148仅能与CCR8结合，而不能与CCR10、CCR11、CXCR6 / BONZO、APJ、DARC或孤儿受体BOB、EBI-II、GPR4、GPR17、HCR或RDC1结合。我们得出结论，MC148是一种高度选择性的CCR8拮抗剂，可以想象它经过优化以干扰自然杀伤细胞和单核细胞的侵袭，而广谱拮抗剂vMIP-II通过阻断多种受体来保护HHV8。