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

Anne H. Cross, Michael J. Ramsbottom, Jeri Anne Lyons

Research output: Contribution to journalArticle

9 Scopus citations

Abstract

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 glycoprotein-immunized 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 tumor necrosis factor. NO plays an important regulatory role in autoimmune T cell induction.

Original languageEnglish
Pages (from-to)79-86
Number of pages8
JournalJournal of Neuroimmunology
Volume173
Issue number1-2
DOIs
StatePublished - Apr 1 2006

Keywords

  • Experimental autoimmune encephalomyelitis
  • Immune regulation
  • Interferon gamma
  • Nitric oxide
  • Tumor necrosis factor-alpha
  • VLA-4

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