Abstract
Studies in multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE) suggest that peripheral monocyte-derived cells (MDCs) are instrumental for disease initiation. MDCs, however, are plastic, and may exert various functions once in the central nervous system (CNS) for prolonged periods. Furthermore, the long-term effect of MDC depletion on continuing axon loss is not known. We show that long-lasting depletion of MDCs, after onset of EAE clinical deficits, is accompanied by decreased CNS infiltration by pathogenic T lymphocytes. Although this treatment does not reverse clinical disease, it prevents worsening of neurological deficits and long-term axonal loss.
Original language | English (US) |
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Pages (from-to) | 36-46 |
Number of pages | 11 |
Journal | Journal of Neuroimmunology |
Volume | 290 |
DOIs | |
State | Published - Jan 15 2016 |
Keywords
- Axonal protection
- Clodronate
- EAE
- Macrophages
- Microglia
- Monocyte-derived cells
ASJC Scopus subject areas
- Immunology
- Clinical Neurology
- Immunology and Allergy
- Neurology