Journal
TRANSLATIONAL IMMUNOLOGY IN ASIA-OCEANIA
Volume 1283, Issue -, Pages 57-66Publisher
BLACKWELL SCIENCE PUBL
DOI: 10.1111/nyas.12118
Keywords
neuromyelitis optica; inflammation; CNS
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Funding
- KKF [B02-12]
- Guthy-Jackson Charitable Foundation
- NIH
- DFG [KO2964/3-2, SFB TR 128/A06, EXC 1010 SyNergy]
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Neuromyelitis optica (NMO) is a debilitating autoimmune inflammatory disease of the central nervous system (CNS) that is distinct from multiple sclerosis (MS). The discovery of NMO-immunoglobulin G (IgG) in the serum of NMO-but not MS-patients was a breakthrough in defining diagnostic criteria for NMO. NMO-IgG is an antibody directed against the astrocytic water channel protein aquaporin-4 (AQP4). While there is evidence that NMO-IgG is also involved in mediating tissue damage in the CNS, many aspects of the pathogenic cascade in NMO remain to be determined. It is clear that antigen-specific T cells contribute to the generation of NMO-IgG in the peripheral immune compartment, as well as to the development of NMO lesions in the CNS. T helper 17 (Th17) cells, equipped both in providing B cell help and inducing tissue inflammation, may be involved in NMO development and pathogenesis. Here, we review immunologic aspects of NMO, placing recent findings in the biology of T-B cell cooperation into perspective with autoimmunity of the CNS.
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