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Immunology of neuromyelitis optica: a T cell-B cell collaboration

Ann N Y Acad Sci. 2013 Apr;1283(1):57-66. doi: 10.1111/nyas.12118

Authors/Editors: Mitsdoerffer M, Kuchroo V, Korn T.
Publication Date: 2013

mitsdoerffer-m-ann-n-y-acadsci-2013

Abstract

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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