The chemokine receptor D6 limits the inflammatory response in vivo

被引：253

作者：

Jamieson, T

Cook, DN

Nibbs, RJB

Rot, A

Nixon, C

Mclean, P

Alcami, A

Lira, SA

Wiekowski, M

Graham, GJ

机构：

[1] Beatson Inst Canc Res, Glasgow G61 1BD, Lanark, Scotland

[2] Duke Univ, Med Ctr, Dept Med, Div Pulm & Crit Care Med, Durham, NC 27706 USA

[3] Univ Glasgow, Div Immunol Infect & Inflammat, Glasgow G11 6NT, Lanark, Scotland

[4] Novartis Inst Biomed Res, A-1230 Vienna, Austria

[5] Univ Glasgow, Dept Vet Pathol, Glasgow G61 1QH, Lanark, Scotland

[6] Univ Autonoma Madrid, Ctr Nacl Biotecnol, Dept Mol & Cellular Biol, E-28049 Madrid, Spain

[7] Mt Sinai Sch Med, Immunobiol Ctr, New York, NY 10029 USA

[8] Schering Plough Corp, Res Inst, Kenilworth, NJ 07033 USA

来源：

NATURE IMMUNOLOGY | 2005年 / 6卷 / 04期

关键词：

D O I：

10.1038/ni1182

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

How the inflammatory response is initiated has been well defined but relatively little is known about how such responses are resolved. Here we show that the D6 chemokine receptor is involved in the post-inflammatory clearance of beta-chemokines from cutaneous sites. After induction of inflammation by phorbol esters, wild-type mice showed a transient inflammatory response. However, in D6-deficient mice, an excess concentration of residual chemokines caused a notable inflammatory pathology with similarities to human psoriasis. These results suggest that D6 is involved in the resolution of the cutaneous inflammatory response.

引用

页码：403 / 411

页数：9

共 51 条

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