The importance of CCR4 and CCR6 in experimental autoimmune encephalomyelitis

被引：22

作者：

Moriguchi, Kota ^{[1
,2
]}

Miyamoto, Katsuichi ^{[3
]}

Tanaka, Noriko ^{[3
]}

Yoshie, Osamu ^{[4
]}

Kusunoki, Susumu ^{[3
]}

机构：

[1] Natl Def Med Coll, Dept Internal Med 3, Div Neurol, Tokorozawa, Saitama 359, Japan

[2] Japan Ground Self Def Force, Middle Army Med Unit, Itami, Hyogo, Japan

[3] Kinki Univ, Sch Med, Dept Neurol, Osaka 5898511, Japan

[4] Kinki Univ, Sch Med, Dept Microbiol, Osaka 5898511, Japan

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2013年 / 257卷 / 1-2期

关键词：

Experimental autoimmune encephalomyelitis; Chemokine receptor; Th17; CCR6; CCR4; T-CELLS; MULTIPLE-SCLEROSIS; EAE; TARGET;

D O I：

10.1016/j.jneuroim.2013.02.002

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Chemokine receptors (CCRs) play important roles in the pathogenesis of immune-mediated diseases, as well as in normal immune response. We examined the role of CCR6 and CCR4 in experimental autoimmune encephalomyelitis (EAE) by using CCR6(-/-)CCR4(-/-) double knockout (DKO) and single knockout mice. DKO mice developed less severe EAE and presented repressed recall response in the induction phase, especially in the activity of T helper 17 (Th17) cells. CCR6 expression in central nervous system (CNS)-infiltrated cells was diminished in DKO. Our results suggest that CCR6 and CCR4 were involved in a more rapid progression of EAE and that their regulation might be a therapeutic target of human inflammatory demyelinating diseases. (C) 2013 Elsevier B.V. All rights reserved.

引用

页码：53 / 58

页数：6

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