IRF-1 signaling in central nervous system glial cells regulates inflammatory demyelination

Zhihua Ren, Yan Wang, David Liebenson, Thomas Liggett, Rajendra Goswami, Dusan Stefoski, Roumen Balabanov*

*Corresponding author for this work

Research output: Contribution to journalArticle

17 Scopus citations

Abstract

The present study provides evidence that interferon regulatory factor 1 (IRF-1) signaling in glial cells is involved in the pathogenesis of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE). Using a bone marrow chimera model of EAE, we demonstrated that CNS IRF-1 regulates inflammatory demyelination and disease severity independently of the peripheral immune cells. In addition, we identified Caspase 1, a pro-inflammatory and pro-apoptotic molecule, as an important transcriptional target of IRF-1. The findings of our study indicate that IRF-1 signaling in glial cells serves as a final common pathway of inflammatory demyelination and may have important clinical implications in MS.

Original languageEnglish (US)
Pages (from-to)147-159
Number of pages13
JournalJournal of Neuroimmunology
Volume233
Issue number1-2
DOIs
StatePublished - Apr 1 2011

Keywords

  • CNS inflammation
  • Caspase 1
  • Experimental autoimmune encephalomyelitis
  • Glial cells
  • Interferon regulatory factor 1
  • Multiple sclerosis

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

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