TY - JOUR
T1 - Neuromyelitis optica-like pathology is dependent on type I interferon response
AU - Khorooshi, Reza
AU - Wlodarczyk, Agnieszka
AU - Asgari, Nasrin
AU - Owens, Trevor
N1 - Available online 20 February 2013
PY - 2013
Y1 - 2013
N2 - 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.
AB - 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.
U2 - 10.1016/j.expneurol.2013.02.005
DO - 10.1016/j.expneurol.2013.02.005
M3 - Journal article
C2 - 23434493
SN - 0014-4886
VL - 247
SP - 744
EP - 747
JO - Experimental Neurology
JF - Experimental Neurology
ER -