Attenuation of experimental autoimmune neuritis in the Lewis rat by treatment with an antibody to L-selectin

被引：11

作者：

Archelos, JJ

Fortwangler, T

Hartung, HP

机构：

[1] UNIV WURZBURG,DEPT NEUROL,CLIN RES GRP MULTIPLE SCLEROSIS,D-97080 WURZBURG,GERMANY

[2] GRAZ UNIV,DEPT NEUROL,A-8036 GRAZ,AUSTRIA

来源：

NEUROSCIENCE LETTERS | 1997年 / 235卷 / 1-2期

关键词：

experimental autoimmune neuritis; autoimmune disease; adhesion molecules; peripheral nervous system; therapy;

D O I：

10.1016/S0304-3940(97)00692-7

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The leukocyte adhesion molecule L-selectin plays a key role in the initial steps of transendothelial migration of T cells and monocytes. In this study we investigated the role of L-selectin in the pathogenesis of experimental autoimmune neuritis (EAN) an animal model of the Guillain-Barre syndrome. EAN was induced in Lewis rats by sensitization with peripheral nerve myelin. Treatment with HRL3, a monoclonal antibody to L-selectin, efficiently suppressed clinical signs of EAN. Histological examination of the peripheral nervous system (PNS) revealed a marked reduction of inflammatory infiltrates and demyelination during treatment with HRL3. We conclude that L-selectin-dependent mechanisms are of pathophysiological relevance in EAN. Modulation of L-selectin in vivo could be a novel therapeutic approach to autoimmune diseases of the PNS. (C) 1997 Elsevier Science Ireland Ltd.

引用

页码：9 / 12

页数：4

共 16 条

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[2]

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