Evidence map›Paper›PMID 38996203›Full record

ReviewNeurology(R) neuroimmunology & neuroinflammation2024

MOG CNS Autoimmunity and MOGAD.

Carson E Moseley, Akash Virupakshaiah, Thomas G Forsthuber, Lawrence Steinman, Emmanuelle Waubant, Scott S Zamvil

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Neurology(R) neuroimmunology & neuroinflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

40 citing papers in PubMed.

  1. Article
  2. MOGAD-Like Encephalitic Syndromes Without MOG Antibodies in Children.Neurology(R) neuroimmunology & neuroinflammation · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. MOGAD Is the Most Common Cause of Isolated Optic Neuritis in Children.Annals of clinical and translational neurology · 2026
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Multi-tracer PET and MR imaging visualize distinct metabolic and inflammatory profiles in the white matter of NMOSD and MOGAD.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Carson E MoseleyFrom the Department of Neurology (C.E.M., A.V., E.W., S.S.Z.), Weill Institute for Neurosciences, University of California, San Francisco; Department of Molecular Microbiology and Immunology (T.G.F.), University of Texas at San Antonio; Department of Neurology and Neurological Science (L.S.), Stanford University; and Program in Immunology (S.S.Z.), University of California, San Francisco, CA.ORCID 0000-0001-8859-3792
Akash VirupakshaiahFrom the Department of Neurology (C.E.M., A.V., E.W., S.S.Z.), Weill Institute for Neurosciences, University of California, San Francisco; Department of Molecular Microbiology and Immunology (T.G.F.), University of Texas at San Antonio; Department of Neurology and Neurological Science (L.S.), Stanford University; and Program in Immunology (S.S.Z.), University of California, San Francisco, CA.ORCID 0000-0003-2624-9974
Thomas G ForsthuberFrom the Department of Neurology (C.E.M., A.V., E.W., S.S.Z.), Weill Institute for Neurosciences, University of California, San Francisco; Department of Molecular Microbiology and Immunology (T.G.F.), University of Texas at San Antonio; Department of Neurology and Neurological Science (L.S.), Stanford University; and Program in Immunology (S.S.Z.), University of California, San Francisco, CA.
Lawrence SteinmanFrom the Department of Neurology (C.E.M., A.V., E.W., S.S.Z.), Weill Institute for Neurosciences, University of California, San Francisco; Department of Molecular Microbiology and Immunology (T.G.F.), University of Texas at San Antonio; Department of Neurology and Neurological Science (L.S.), Stanford University; and Program in Immunology (S.S.Z.), University of California, San Francisco, CA.
Emmanuelle WaubantFrom the Department of Neurology (C.E.M., A.V., E.W., S.S.Z.), Weill Institute for Neurosciences, University of California, San Francisco; Department of Molecular Microbiology and Immunology (T.G.F.), University of Texas at San Antonio; Department of Neurology and Neurological Science (L.S.), Stanford University; and Program in Immunology (S.S.Z.), University of California, San Francisco, CA.ORCID 0000-0001-5188-0157
Scott S ZamvilFrom the Department of Neurology (C.E.M., A.V., E.W., S.S.Z.), Weill Institute for Neurosciences, University of California, San Francisco; Department of Molecular Microbiology and Immunology (T.G.F.), University of Texas at San Antonio; Department of Neurology and Neurological Science (L.S.), Stanford University; and Program in Immunology (S.S.Z.), University of California, San Francisco, CA.ORCID 0000-0003-2720-9915

Funding

Characterization of T cells in MOG antibody-associated diseaseR01AI170863 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SCOTT S ZAMVIL · 2023 to 2026
$3.2M
NIAID NIH HHS R01 AI170863
6 · The paper itself

Abstract

At one time considered a possible form of neuromyelitis optica (NMO) spectrum disorder (NMOSD), it is now accepted that myelin oligodendrocyte glycoprotein (MOG) antibody (Ab)-associated disorder (MOGAD) is a distinct entity from either NMO or multiple sclerosis (MS) and represents a broad spectrum of clinical phenotypes. Whereas Abs targeting aquaporin-4 (AQP4) in NMO are pathogenic, the extent that anti-MOG Abs contribute to CNS damage in MOGAD is unclear. Both AQP4-specific Abs in NMO and MOG-specific Abs in MOGAD are predominantly IgG1, a T cell-dependent immunoglobulin (Ig) subclass. Key insights in neuroimmunology and MOGAD pathogenesis have been learned from MOG experimental autoimmune encephalomyelitis (EAE), described 2 decades before the term MOGAD was introduced. MOG-specific T cells are required in MOG EAE, and while anti-MOG Abs can exacerbate EAE and CNS demyelination, those Abs are neither necessary nor sufficient to cause EAE. Knowledge regarding the spectrum of MOGAD clinical and radiologic presentations is advancing rapidly, yet our grasp of MOGAD pathogenesis is incomplete. Understanding both the humoral and cellular immunology of MOGAD has implications for diagnosis, treatment, and prognosis.

Indexed as

AutoantibodiesMyelin-Oligodendrocyte GlycoproteinNeuromyelitis OpticaAnimalsAutoimmunityDemyelinating Autoimmune Diseases, CNSEncephalomyelitis, Autoimmune, ExperimentalHumansAutoantibodiesMOG protein, humanMyelin-Oligodendrocyte Glycoprotein

Identifiers

PMID38996203
PMCPMC11256982

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.