Abstract
Inflammatory signals present in demyelinated multiple sclerosis lesions affect the reparative remyelination process conducted by oligodendrocyte progenitor cells (OPCs). Interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), and interleukin (IL)-6 have differing effects on the viability and growth of OPCs, however the effects of IL-17A are largely unknown. Primary murine OPCs were stimulated with IL-17A and their viability, proliferation, and maturation were assessed in culture. IL-17A-stimulated OPCs exited the cell cycle and differentiated with no loss in viability. Expression of the myelin-specific protein, proteolipid protein, increased in a cerebellar slice culture assay in the presence of IL-17A. Downstream, IL-17A activated ERK1/2 within 15 min and induced chemokine expression in 2 days. These results demonstrate that IL-17A exposure stimulates OPCs to mature and participate in the inflammatory response.
Original language | English (US) |
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Pages (from-to) | 768-779 |
Number of pages | 12 |
Journal | Glia |
Volume | 63 |
Issue number | 5 |
DOIs | |
State | Published - May 1 2015 |
Keywords
- Chemokine
- ERK
- Inflammation
- Interleukin-17
- Myelin
- Oligodendrocyte
ASJC Scopus subject areas
- Neurology
- Cellular and Molecular Neuroscience