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.

• Authors: Reza Khorooshi, Agnieszka Wlodarczyk, Nasrin Asgari, Trevor Owens
• Journal: Experimental neurology (Exp Neurol) Vol. 247 Pg. 744-7 (Sep 2013) ISSN: 1090-2430 [Electronic] United States
• PMID: 23434493 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2013 Elsevier Inc. All rights reserved.

Chemical References

• Aif1 protein, mouse
• Aquaporin 4
• Calcium-Binding Proteins
• Complement Membrane Attack Complex
• Glial Fibrillary Acidic Protein
• Immunoglobulin G
• Microfilament Proteins
• Receptor, Interferon alpha-beta
• Complement System Proteins

Topics

• Animals
• Aquaporin 4 (metabolism)
• Calcium-Binding Proteins (metabolism)
• Complement Membrane Attack Complex (metabolism)
• Complement System Proteins (toxicity)
• Disease Models, Animal
• Female
• Gene Expression Regulation (drug effects, genetics)
• Glial Fibrillary Acidic Protein (metabolism)
• Humans
• Immunoglobulin G (toxicity)
• Mice
• Mice, Inbred C57BL
• Mice, Knockout
• Microfilament Proteins (metabolism)
• Neuromyelitis Optica (chemically induced, immunology, pathology)
• Receptor, Interferon alpha-beta (deficiency, metabolism)
• Signal Transduction (drug effects, genetics)