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

Abstract

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.

Keywords: AQP4; Aquaporin-4; Astrocytes; CNS; C′; EAE; GFAP; H&E; IFN alpha/beta receptor; IFNAR; Inflammation; LFB; MS; NMO; Neuromyelitis optica; Type I IFN; aquaporin-4; central nervous system; complement; experimental autoimmune encephalomyelitis; glial fibrillary acidic protein; hematoxylin and eosin; luxol fast blue; multiple sclerosis; neuromyelitis optica.