Evidence map›Paper›PMID 42908053›Full record

ArticleAnnals of clinical and translational neurology2026

Investigation of Complement Activation and Cytokine Signatures in AQP4+ NMOSD, MOGAD, and MS.

Angeliki G Filippatou, Susana Dominguez-Penuela, David Acero-Garces, Georgios Gakis, Matthew D Smith, Yasmin Resto, Maria Reyes-Mantilla, Haiwen Chen, Isabella Hernandez, Yana Said and 14 more

Abstract read
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In one paragraph

Article in Annals of clinical and translational neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

24 authors.

Angeliki G FilippatouDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID https://orcid.org/0000-0003-0419-233X
Susana Dominguez-PenuelaDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
David Acero-GarcesDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID https://orcid.org/0000-0002-9717-4626
Georgios GakisDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID https://orcid.org/0000-0002-7339-4659
Matthew D SmithDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Yasmin RestoDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Maria Reyes-MantillaDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Haiwen ChenDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Isabella HernandezDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Yana SaidDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID https://orcid.org/0009-0004-4350-1910
Andrea Salazar-CameloDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Christina HuynhAnnexon Biosciences, Brisbane, California, USA.
Alessia TassoniAnnexon Biosciences, Brisbane, California, USA.
Ted YednockAnnexon Biosciences, Brisbane, California, USA.
Rick ArtisAnnexon Biosciences, Brisbane, California, USA.
Yaisa Andrews-ZwillingAnnexon Biosciences, Brisbane, California, USA.
Scott D NewsomeDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Shiv SaidhaDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Pavan BhargavaDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID https://orcid.org/0000-0002-7947-9418
Ellen M MowryDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Kathryn C FitzgeraldDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID https://orcid.org/0000-0003-3137-0322
Peter A CalabresiDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Carlos A PardoDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID https://orcid.org/0000-0002-4128-5335
Elias S SotirchosDepartment of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID https://orcid.org/0000-0002-8812-1637

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveAquaporin-4-IgG seropositive neuromyelitis optica spectrum disorder (AQP4+ NMOSD), myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), and multiple sclerosis (MS) are pathophysiologically distinct neuroinflammatory disorders. Complement activation is a major mechanism of injury in AQP4+ NMOSD, whereas its role in MS is complex and in MOGAD controversial. We aimed to compare complement components and cytokines between AQP4+ NMOSD, MOGAD, and MS.

methodsCSF complement components, CSF and plasma cytokines, neurofilament light chain (NfL) and glial fibrillary acidic protein (GFAP) were measured in people with AQP4+ NMOSD (CSF: n = 19; plasma: n = 18), MOGAD (CSF: n = 29; plasma: n = 35) and MS (CSF: n = 36; plasma: n = 58) with recent disease activity. Controls included subjects with non-inflammatory conditions (CSF: n = 51) and healthy controls (plasma: n = 29).

resultsCSF IL-10 and TNF-a were elevated across all neuroinflammatory disease groups relative to controls. CSF IL-6 was elevated only in AQP4+ NMOSD and MOGAD. There were no significant differences in plasma cytokines between groups. Most complement components were elevated in AQP4+ NMOSD and MOGAD; only specific activation products (C2b, C3d, C4a, C5a) were elevated in MS. CSF GFAP and NfL correlated with several CSF cytokines and complement components in AQP4+ NMOSD and MOGAD. Expanded Disability Status Scale at nadir during attacks correlated with CSF BAFF, GFAP, free C1q, C1s, C1s-C1inh, C4a in AQP4+ NMOSD, and CSF IL-10, TNF-a, free C1q, C1inh, C4a in MOGAD.

interpretationOur findings suggest distinct CSF cytokine profiles in AQP4+ NMOSD, MOGAD, and MS, and widespread activation of complement pathways in AQP4+ NMOSD and MOGAD. CSF complement and cytokine profiling may help characterize neuroinflammatory disease mechanisms, although further validation of these findings in larger cohorts is needed.

Indexed as

complementcytokinesmogadmultiple sclerosisneuromyelitis optica

Identifiers

PMID42908053
PMCPMC13687446

What OpenQuestion holds

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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.