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 language | English (US) |
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Pages (from-to) | 147-159 |
Number of pages | 13 |
Journal | Journal of Neuroimmunology |
Volume | 233 |
Issue number | 1-2 |
DOIs | |
State | Published - Apr 2011 |
Keywords
- CNS inflammation
- Caspase 1
- Experimental autoimmune encephalomyelitis
- Glial cells
- Interferon regulatory factor 1
- Multiple sclerosis
ASJC Scopus subject areas
- Clinical Neurology
- Neurology
- Immunology and Allergy
- Immunology