Evidence map›Paper›PMID 27435215›Full record

ArticleScientific reports2016

CEACAM1 mediates B cell aggregation in central nervous system autoimmunity.

Damiano M Rovituso, Laura Scheffler, Marie Wunsch, Christoph Kleinschnitz, Sebastian Dörck, Jochen Ulzheimer, Antonios Bayas, Lawrence Steinman, Süleyman Ergün, Stefanie Kuerten

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.4field-weighted citation impact, top 18% of its field
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

8 citing papers in PubMed, 22 citations in OpenAlex.

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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

10 authors at 6 institutions in 2 countries.

Damiano M RovitusoDepartment of Anatomy and Cell Biology, University of Würzburg, Würzburg, Germany.
Laura SchefflerDepartment of Anatomy and Cell Biology, University of Würzburg, Würzburg, Germany.
Marie WunschDepartment of Anatomy and Cell Biology, University of Würzburg, Würzburg, Germany.
Christoph KleinschnitzDepartment of Neurology, University Hospitals of Würzburg, Würzburg, Germany.
Sebastian DörckDepartment of Neurology, University Hospitals of Würzburg, Würzburg, Germany.
Jochen UlzheimerDepartment of Neurology, Caritas-Krankenhaus Bad Mergentheim, Bad Mergentheim, Germany.
Antonios BayasDepartment of Neurology, Klinikum Augsburg, Augsburg, Germany.
Lawrence SteinmanDepartment of Neurology, Stanford University School of Medicine, Palo Alto, CA, USA.
Süleyman ErgünDepartment of Anatomy and Cell Biology, University of Würzburg, Würzburg, Germany.
Stefanie KuertenDepartment of Anatomy and Cell Biology, University of Würzburg, Würzburg, Germany.
University of Würzburg · DECaritas-Krankenhaus Bad Mergentheim · DEEssen University Hospital · DEStanford University · USUniversitätsklinikum Würzburg · DEUniversity Hospital Augsburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

B cell aggregates in the central nervous system (CNS) have been associated with rapid disease progression in patients with multiple sclerosis (MS). Here we demonstrate a key role of carcinoembryogenic antigen-related cell adhesion molecule1 (CEACAM1) in B cell aggregate formation in MS patients and a B cell-dependent mouse model of MS. CEACAM1 expression was increased on peripheral blood B cells and CEACAM1(+) B cells were present in brain infiltrates of MS patients. Administration of the anti-CEACAM1 antibody T84.1 was efficient in blocking aggregation of B cells derived from MS patients. Along these lines, application of the monoclonal anti-CEACAM1 antibody mCC1 was able to inhibit CNS B cell aggregate formation and significantly attenuated established MS-like disease in mice in the absence of any adverse effects. CEACAM1 was co-expressed with the regulator molecule T cell immunoglobulin and mucin domain -3 (TIM-3) on B cells, a novel molecule that has recently been described to induce anergy in T cells. Interestingly, elevated coexpression on B cells coincided with an autoreactive T helper cell phenotype in MS patients. Overall, these data identify CEACAM1 as a clinically highly interesting target in MS pathogenesis and open new therapeutic avenues for the treatment of the disease.

Indexed as

AnimalsAntibodies, Anti-IdiotypicAntigens, CDAutoimmunityB-LymphocytesCell AdhesionCell Adhesion MoleculesCell AggregationCentral Nervous SystemDisease Models, AnimalGene Expression RegulationHumansLymphocyte ActivationMiceMultiple SclerosisAntibodies, Anti-IdiotypicAntigens, CDCD66 antigensCell Adhesion Molecules

Identifiers

PMID27435215
PMCPMC4951702
OpenAlexW2504197513

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.