Evidence map›Paper›PMID 39981242›Full record

ArticleFrontiers in immunology2025

Assessing the inflammation in pediatric MOGAD: Significance of CSF HMGB1 and related biomarkers.

Xin Wang, Ruibin Zhao, Jiayu Fan, Chong Liu, Li Zhang, Huafang Yang, Weiyi Wang

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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. Cited by 1 paper.

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

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Xin WangSecond Department of Neurology, Hebei Children's Hospital, Shijiazhuang, China.
Ruibin ZhaoSchool of Medical Imaging, Hebei Medical University, Shijiazhuang, China.
Jiayu FanSecond Department of Neurology, Hebei Children's Hospital, Shijiazhuang, China.
Chong LiuSecond Department of Neurology, Hebei Children's Hospital, Shijiazhuang, China.
Li ZhangDepartment of Pathology, Hebei Children's Hospital, Shijiazhuang, China.
Huafang YangSecond Department of Neurology, Hebei Children's Hospital, Shijiazhuang, China.
Weiyi WangSecond Department of Neurology, Hebei Children's Hospital, Shijiazhuang, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background and purpose: Myelin-oligodendrocyte glycoprotein antibody associated disease (MOGAD) is a common inflammatory disease of the central nervous system (CNS) in children that can lead to demyelination. Evaluation and monitoring of biomarkers associated with its pathogenesis would provide vital information on disease progression and therapeutic assessment. Methods: We assessed NLRP3, HMGB1, IL-6, and IL-33 levels in the cerebrospinal fluid (CSF) of pediatric patients with MOGAD at different time points and their association with the risk of disease. We recruited 30 patients with MOGAD (20 in the acute phase and 10 in remission) and 10 control patients with noninflammatory demyelinating disease. The expanded disability status scale (EDSS) was used to assess disease severity. Results: NLRP3, HMGB1, and IL-6 levels in the CSF were significantly higher in patients with MOGAD during the acute phase than in remission ( Conclusions: These findings suggest that NLRP3, HMGB1, and IL-6 in the CSF may be potential therapeutic targets and are at least partly involved in the pathogenesis of pediatric MOGAD. HMGB1 in the CSF may be a potential biomarker correlating with pediatric MOGAD severity. Further investigations are warranted to validate potential cytokine pathways between that NLRP3, HMGB1, and IL-6 of MOGAD.

Indexed as

Demyelinating DiseasesHMGB1 ProteinInflammationAdolescentAutoantibodiesBiomarkersChildChild, PreschoolFemaleHumansInterleukin-33Interleukin-6MaleMyelin-Oligodendrocyte GlycoproteinMyelin Oligodendrocyte Glycoprotein Antibody-Associated DiseaseNLR Family, Pyrin Domain-Containing 3 ProteinAutoantibodiesBiomarkersHMGB1 ProteinHMGB1 protein, humanIL33 protein, humanIL6 protein, humanInterleukin-33Interleukin-6MOG protein, humanMyelin-Oligodendrocyte GlycoproteinNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanCSFHMGB1IL-6MOGADNLRP3pediatric

Identifiers

PMID39981242
PMCPMC11839407

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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.