Evidence map›Paper›PMID 38889374›Full record

ArticleNeurology(R) neuroimmunology & neuroinflammation2024

Interleukin-6 Signaling Blockade Induces Regulatory Plasmablasts in Neuromyelitis Optica Spectrum Disorder.

Ritsu Akatani, Norio Chihara, Atsushi Hara, Asato Tsuji, Shusuke Koto, Kazuhiro Kobayashi, Tatsushi Toda, Riki Matsumoto

Abstract read
In one paragraph

Article 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 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

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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

5 citing papers in PubMed.

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  5. Review
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

8 authors.

Ritsu AkataniFrom the Division of Neurology (R.A., N.C., A.H., A.T., S.K., R.M.); Division of Molecular Brain Science (K.K.), Kobe University Graduate School of Medicine; and Department of Neurology (T.T.), Graduate School of Medicine, The University of Tokyo, Japan.ORCID 0000-0003-3982-1108
Norio ChiharaFrom the Division of Neurology (R.A., N.C., A.H., A.T., S.K., R.M.); Division of Molecular Brain Science (K.K.), Kobe University Graduate School of Medicine; and Department of Neurology (T.T.), Graduate School of Medicine, The University of Tokyo, Japan.ORCID 0000-0003-4499-0790
Atsushi HaraFrom the Division of Neurology (R.A., N.C., A.H., A.T., S.K., R.M.); Division of Molecular Brain Science (K.K.), Kobe University Graduate School of Medicine; and Department of Neurology (T.T.), Graduate School of Medicine, The University of Tokyo, Japan.
Asato TsujiFrom the Division of Neurology (R.A., N.C., A.H., A.T., S.K., R.M.); Division of Molecular Brain Science (K.K.), Kobe University Graduate School of Medicine; and Department of Neurology (T.T.), Graduate School of Medicine, The University of Tokyo, Japan.
Shusuke KotoFrom the Division of Neurology (R.A., N.C., A.H., A.T., S.K., R.M.); Division of Molecular Brain Science (K.K.), Kobe University Graduate School of Medicine; and Department of Neurology (T.T.), Graduate School of Medicine, The University of Tokyo, Japan.
Kazuhiro KobayashiFrom the Division of Neurology (R.A., N.C., A.H., A.T., S.K., R.M.); Division of Molecular Brain Science (K.K.), Kobe University Graduate School of Medicine; and Department of Neurology (T.T.), Graduate School of Medicine, The University of Tokyo, Japan.
Tatsushi TodaFrom the Division of Neurology (R.A., N.C., A.H., A.T., S.K., R.M.); Division of Molecular Brain Science (K.K.), Kobe University Graduate School of Medicine; and Department of Neurology (T.T.), Graduate School of Medicine, The University of Tokyo, Japan.ORCID 0000-0002-0717-1123
Riki MatsumotoFrom the Division of Neurology (R.A., N.C., A.H., A.T., S.K., R.M.); Division of Molecular Brain Science (K.K.), Kobe University Graduate School of Medicine; and Department of Neurology (T.T.), Graduate School of Medicine, The University of Tokyo, Japan.ORCID 0000-0003-3985-9210

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

objectivesInterleukin-6 receptor antibodies (IL-6R Abs), including satralizumab, are increasingly used to prevent relapse for neuromyelitis optica spectrum disorder (NMOSD). However, the detailed mechanism of action of this treatment on the lymphocyte phenotype remains unclear. This study focused on B cells in patients with NMOSD, hypothesizing that IL-6R Ab enables B cells to acquire regulatory functions by producing the anti-inflammatory cytokine IL-10.

methodsPeripheral blood mononuclear cells were stimulated in vitro to induce the expansion of B-cell subsets, double-negative B cells (DNs; CD19

resultsDNs and PBs were observed to expand in patients with NMSOD during the acute attacks. In the in vitro model, IL-6R Ab increased IL-10 expression in B cells. Notably, IL-10 expression increased in PBs but not in DNs. Using RNA sequencing, CD200 was identified as a marker of regulatory PBs among the differentially expressed upregulated genes. CD200 DISCUSSION: Treatment with IL-6 signaling blockade elicited a regulatory phenotype in B cells and PBs. CD200

Indexed as

Interleukin-6Neuromyelitis OpticaReceptors, Interleukin-6AdultFemaleHumansInterleukin-10MaleMiddle AgedPlasma CellsSignal TransductionIL10 protein, humanIL6 protein, humanInterleukin-10Interleukin-6Receptors, Interleukin-6

Identifiers

PMID38889374
PMCPMC11188987

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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.