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Immunology of neuromyelitis optica: a T cell–B cell collaboration
Author(s) -
Mitsdoerffer Meike,
Kuchroo Vijay,
Korn Thomas
Publication year - 2013
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/nyas.12118
Subject(s) - neuromyelitis optica , immunology , multiple sclerosis , autoimmunity , antibody , immune system , aquaporin 4 , experimental autoimmune encephalomyelitis , medicine , biology , pathology
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.