Influence of type I IFN signaling on anti-MOG antibody-mediated demyelination.

Carsten Tue BergReza KhorooshiNasrin AsgariTrevor Owens

Published in: Journal of neuroinflammation (2017)

Anti-MOG antibody and complement was sufficient to induce callosal demyelination, and pathology was dependent on type I IFN. Induction of EAE in IFNAR1-KO mice overcame the dependence on type I IFN for anti-MOG and complement-mediated demyelination.

Keyphrases

immune response
dendritic cells
metabolic syndrome
high fat diet induced
adipose tissue
insulin resistance
skeletal muscle
spectrum disorder