IL-12 driven upregulation of P-selectin ligand on myelin-specific T cells is a critical step in an animal model of autoimmune demyelination

被引:25
作者
Deshpande, P
King, IL
Segal, BM
机构
[1] Univ Rochester, Sch Med & Dent, Dept Neurol, Rochester, NY 14642 USA
[2] Univ Rochester, Sch Med & Dent, Dept Microbiol & Immunol, Rochester, NY 14642 USA
[3] Univ Rochester, Sch Med & Dent, Ctr Canc, Rochester, NY 14642 USA
[4] Univ Rochester, Sch Med & Dent, Interdept Grad Program Neurosci, Rochester, NY 14642 USA
关键词
experimental autoimmune encephalomyelitis; interleukin-12; cytokines; Th1; cells; P-selectin ligand; adhesion molecules; multiple sclerosis;
D O I
10.1016/j.jneuroim.2005.11.016
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Experimental autoimmune encephalomyelitis (EAE) is an inflammatory demyelinating disease of the central nervous system. IL-12p40 rrionokines play a critical role in the generation of EAE-inducing CD4+T cells. Here we show that IL-12 directly upregulates the expression of the adhesion molecule, P-selectin glycoprotein ligand (PSGL-1), on B10.PL MBP-TCR transgenic T cells during their initial encounter with antigen. Pre-incubation of IL-12-stimulated myelin-reactive CD4+T cells with a blocking antibody against PSGL-1 reduced the incidence and severity of EAE. We conclude that IL-12-driven PSGL-1 expression can facilitate the development of autoimmune demyelination. (c) 2005 Elsevier B.V. All rights reserved.
引用
收藏
页码:35 / 44
页数:10
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