Cited by 91Multiple Sclerosis Research StudiesPeripheral Neuropathies and DisordersOcular Diseases and Behçet’s Syndrome

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

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Mitsdoerffer, Meike, Kuchroo, Vijay, Korn, Thomas·2013·Annals of the New York Academy of Sciences

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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  • Pro-inflammatory autoantigen-specific CD4+ T helper (auto-Th) cells are central orchestrators of autoimmune diseases (AIDs).

    “Pro-inflammatory autoantigen-specific CD4 + Thelper (auto-Th) cells are central orchestrators of autoimmune diseases (AIDs).”

    From Autoantigen-specific CD4+ T cells acquire an exhausted phenotype and persist in human antigen-specific autoimmune diseases (2024) · cites this paper as [3]

    The 'T cell specificity in NMO' section describes an important role for autoantigen-specific effector T cells in NMO, and 'T cell phenotype in NMO' links dysregulated Th1 and Th17 responses to organ-specific autoimmunity. The paper does not establish that these cells are central orchestrators of autoimmune diseases generally; it frames some of its conclusions about NMO as possibilities. Page numbers are unavailable in our copy. (LLM, conf=0.84)

    Experimental — accuracy not yet measured
  • Auto-Th cells orchestrate autoimmune disease via pro-inflammatory cytokines and B cell help, resulting in autoantibody production, as demonstrated in animal models.

    “This process is orchestrated by autoantigen-specific CD4 + T helper (autoTh) cells via pro-inflammatory cytokines and B cell help, resulting in autoantibody production, 1-3 as demonstrated in multiple animal models of AIDs.”

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Authors
Mitsdoerffer, M., Kuchroo, V., & Korn, T.
Affiliations
  • TUM Klinikum (DE)
  • Brigham and Women's Hospital (US)
Corresponding author
Korn, Thomas
Venue
Annals of the New York Academy of Sciences
Publisher
Wiley
Published
2013-04
Volume
1283
Issue
1
Pages
57-66
ISSN
  • 0077-8923 (ISSN-L)
  • 1749-6632
OpenAlex
W1893466103
Cited by
91
References
94
Citations by year
2026: 7 · 2025: 10 · 2024: 6 · 2023: 4 · 2022: 2 · 2021: 9 · 2020: 12 · 2019: 8 · 2018: 5 · 2017: 6 · 2016: 8 · 2015: 5 · 2014: 6 · 2013: 3
FWCI
1.08
Type
journal article
Language
en
Open access
Locations
  • Annals of the New York Academy of Sciences (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
  • mediaTUM (Technical University of Munich) (submittedVersion)
Funders
National Institute of Allergy and Infectious Diseases (R01AI044880)
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
  • Health Sciences › Medicine › Neurology › Peripheral Neuropathies and Disorders
  • Health Sciences › Medicine › Ophthalmology › Ocular Diseases and Behçet’s Syndrome
Keywords
neuromyelitis optica, aquaporin-4 antibodies, aquaporin-4, T cell-B cell cooperation, Th17 cells, neuroinflammation, autoantibody pathogenesis, multiple sclerosis
MeSH terms
Animals, Disease Models, Animal, Humans, Lymphocyte Cooperation, Neuromyelitis Optica, B-Lymphocyte Subsets, T-Lymphocyte Subsets, Mice

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