IL ‐17 A activates ERK 1/2 and enhances differentiation of oligodendrocyte progenitor cells

• Published in: Glia 2015-05, Vol.63 (5), p.768-779
• Main Authors: Rodgers, Jane M., Robinson, Andrew P., Rosler, Elen S., Lariosa‐Willingham, Karen, Persons, Rachael E., Dugas, Jason C., Miller, Stephen D.
• Format: Article
• Language: English
• ISSN: 0894-1491; 1098-1136
• DOI: 10.1002/glia.22783

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. GLIA 2015;63:768–779 IL‐17A ‐stimulated oligodendrocyte progenitor cells exited the cell cycle and differentiated with no loss in viability. Oligodendrocyte progenitor cells also activated ERK and upregulated several cytokine and chemokines in response to IL‐17A stimulation. These data suggest that oligodendrocyte progenitor cells are encouraged to mature while they participate in the inflammatory response to IL‐17A.