Evidence map›Paper›PMID 40777014›Full record

ArticleFrontiers in immunology2025

Reduced tolerogenic factor sCD83 in NMOSD and relapsing MOGAD: a potential new therapeutic pathway.

Ariel Rechtman, Omri Zveik, Lyne Shweiki, Garrick Hoichman, Tal Friedman-Korn, Livnat Brill, Adi Vaknin-Dembinsky

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Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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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

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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

7 authors.

Ariel RechtmanDepartment of Neurology and Laboratory of Neuroimmunology and the Agnes-Ginges Center for Neurogenetics, Hadassah-Hebrew University Medical Center, Ein-Kerem, Jerusalem, Israel.
Omri ZveikDepartment of Neurology and Laboratory of Neuroimmunology and the Agnes-Ginges Center for Neurogenetics, Hadassah-Hebrew University Medical Center, Ein-Kerem, Jerusalem, Israel.
Lyne ShweikiDepartment of Neurology and Laboratory of Neuroimmunology and the Agnes-Ginges Center for Neurogenetics, Hadassah-Hebrew University Medical Center, Ein-Kerem, Jerusalem, Israel.
Garrick HoichmanDepartment of Neurology and Laboratory of Neuroimmunology and the Agnes-Ginges Center for Neurogenetics, Hadassah-Hebrew University Medical Center, Ein-Kerem, Jerusalem, Israel.
Tal Friedman-KornDepartment of Neurology and Laboratory of Neuroimmunology and the Agnes-Ginges Center for Neurogenetics, Hadassah-Hebrew University Medical Center, Ein-Kerem, Jerusalem, Israel.
Livnat Brill *Department of Neurology and Laboratory of Neuroimmunology and the Agnes-Ginges Center for Neurogenetics, Hadassah-Hebrew University Medical Center, Ein-Kerem, Jerusalem, Israel.
Adi Vaknin-Dembinsky *Department of Neurology and Laboratory of Neuroimmunology and the Agnes-Ginges Center for Neurogenetics, Hadassah-Hebrew University Medical Center, Ein-Kerem, Jerusalem, Israel.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Neuromyelitis optica spectrum disorders (NMOSD) and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) are autoimmune central nervous system disorders with poorly understood immune pathways. CD83 plays a crucial role in the development and maintenance of immune tolerance. This study aims to evaluate CD83 expression in NMOSD and MOGAD and its correlation with disease activity. Methods: RNA extracted from PBMCs of MOGAD, NMOSD and healthy controls (HCs) was analyzed to assess CD83 expression levels. ELISA was used to quantify soluble CD83 (sCD83) levels in the CSF and serum of patients. Additionally, the effects of therapeutic agents used for CNS demyelinating diseases on sCD83 expression levels were examined. The study enrolled 231 untreated participants, including 64 with MOGAD, 56 with NMOSD, 47 with MS, and 64 HCs. Results: NMOSD patients exhibited lower sCD83 levels compared to MOGAD and HCs, and MOGAD patients with a relapsing course had lower sCD83 levels than those with a monophasic course. Lower sCD83 levels correlated with a severe disease course. Treatment with IVIG and azathioprine significantly increased sCD83 levels in the patients' serum. Discussion: Our study consistently found lower sCD83 levels in NMOSD and relapsing MOGAD patients. sCD83 levels increased following IVIG and immunosuppressive therapy. This elevation may reflect either a direct effect of the therapy itself, or a compensatory rebound response following immune suppression. These findings highlight the potential of sCD83 as a prognostic biomarker in these diseases and support its role as both a therapeutic target and a marker for treatment response in CNS demyelinating disorders.

Indexed as

Antigens, CDImmune ToleranceImmunoglobulinsMembrane GlycoproteinsMyelin Oligodendrocyte Glycoprotein Antibody-Associated DiseaseNeuromyelitis OpticaAdultAutoantibodiesBiomarkersCD83 AntigenFemaleHumansImmunoglobulins, IntravenousImmunosuppressive AgentsMaleMiddle AgedAntigens, CDAutoantibodiesBiomarkersCD83 AntigenImmunoglobulinsImmunoglobulins, IntravenousImmunosuppressive AgentsMembrane GlycoproteinsazathioprineCD83demyelinating CNS diseaseIVIgMOGADmycophenolate mofetilNMOSDsoluble CD83

Identifiers

PMID40777014
PMCPMC12328149

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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.