Journal
JOURNAL OF NEUROIMMUNOLOGY
Volume 173, Issue 1-2, Pages 79-86Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jneuroim.2005.11.022
Keywords
nitric oxide; experimental autoimmune encephalomyelitis; immune regulation; VLA-4; interferon gamma; tumor necrosis factor-alpha
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Funding
- NINDS NIH HHS [R01 NS37037] Funding Source: Medline
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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.
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