NOS2 regulates cytokine production and VLA-4 expression in experimental autoimmune encephalomyelitis

被引：8

作者：

Cross, AH ^{[1
]}

Ramsbottom, MJ ^{[1
]}

Lyons, JA ^{[1
]}

机构：

[1] Washington Univ, Sch Med, Dept Neurol & Neurosurg, St Louis, MO 63110 USA

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2006年 / 173卷 / 1-2期

关键词：

nitric oxide; experimental autoimmune encephalomyelitis; immune regulation; VLA-4; interferon gamma; tumor necrosis factor-alpha;

D O I：

10.1016/j.jneuroim.2005.11.022

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Inducible nitric oxide synthase (NOS2) expression in the central nervous system correlates with EAE disease activity. Inhibition of NOS2 ameliorates adoptively transferred EAE, yet exacerbates actively induced EAE. Herein, the encephalitogenicity of T cells induced by immunization in the presence or absence of NOS2 was examined. Upon passive transfer, T cells from myelin oligodendrocyte glycoproteinimmunized NOS2-deficient C57BL/6 mice induced more severe EAE than T cells from wild-type mice. The heightened encephalitogenicity of NOS2-/- T cells Correlated with enhanced expression of VLA-4 (CD49d) and increased production of interferon gamma and turnor necrosis factor. NO plays an important regulatory role in autoimmune T cell induction. (c) 2006 Published by Elsevier B.V.

引用

页码：79 / 86

页数：8

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