Bone marrow-derived versus parenchymal sources of inducible nitric oxide synthase in experimental autoimmune encephalomyelitis

被引：14

作者：

Zehntner, SP

Bourbonniere, L

Hassan-Zahraee, M

Tran, E

Owens, T

机构：

[1] Montreal Neurol Inst, Neuroimmunol Unit, Montreal, PQ H3A 3B4, Canada

[2] Antigen Inc, Woburn, MA 01801 USA

[3] Yale Univ, Howard Hughes Med Inst, Dept Immunol, New Haven, CT 06520 USA

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2004年 / 150卷 / 1-2期

基金：

加拿大健康研究院;

关键词：

EAE; nitric oxide; radiation chimeras; superoxide; delayed onset;

D O I：

10.1016/j.jneuroim.2004.01.020

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

The role of nitric oxide (NO) in central nervous system (CNS) inflammation is uncertain. Whereas experimental autoimmune encephalomyelitis (EAE) is exacerbated in mice deficient in inducible nitric oxide synthase (iNOS), inhibitor studies have suggested a pro-inflammatory role for NO. These discrepancies may reflect balance between immunoregulatory and neurocytopathologic roles for NO. We investigated selective effects of bone marrow-derived versus CNS parenchymal sources of iNOS in EAE in chimeric mice. Chimeras that selectively expressed or ablated iNOS in leukocytes both showed significant delay in disease onset, with no difference in disease severity. We conclude that bone marrow-derived and CNS parenchymal sources of iNOS-derived NO both play a regulatory role in EAE. (C) 2004 Elsevier B.V. All rights reserved.

引用

页码：70 / 79

页数：10

共 58 条

[31] Interactions between hemopoietically derived TNF and central nervous system-resident glial chemokines underlie initiation of autoimmune inflammation in the brain [J].