Neuromyelitis optica-like pathology is dependent on type I interferon response

Reza Khorooshi, Agnieszka Wlodarczyk, Nasrin Asgari, Trevor Owens*

*Corresponding author af dette arbejde

    Publikation: Bidrag til tidsskriftArtikelForskningpeer review


    Neuromyelitis optica is an antibody-mediated autoimmune inflammatory disease of the central nervous system. Reports have suggested that interferon beta which is beneficial for multiple sclerosis, exacerbates neuromyelitis optica. Our aim was to determine whether type I interferon plays a role in the formation of neuromyelitis optica lesions. Immunoglobulin G from a neuromyelitis optica patient was injected intracerebrally with human complement to type I interferon receptor deficient and wildtype mice. Loss of aquaporin-4 and glial fibrillary acidic protein was reduced in type I interferon receptor deficient mice brain. Our findings suggest that type I interferon signaling contributes to neuromyelitis optica pathogenesis.

    Sider (fra-til)744-747
    Antal sider4
    TidsskriftExperimental Neurology
    StatusUdgivet - 1 sep. 2013


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