Evidence map›Paper›PMID 30087255›Full record

ArticleInternational journal of molecular sciences2018

CTLA-4 Mediates Inhibitory Function of Mesenchymal Stem/Stromal Cells.

Timo Gaber, Kerstin Schönbeck, Holger Hoff, Cam Loan Tran, Cindy Strehl, Annemarie Lang, Sarah Ohrndorf, Moritz Pfeiffenberger, Eric Röhner, Georg Matziolis and 3 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

33 citing papers in PubMed, 44 citations in OpenAlex.

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  15. Checkpoint Inhibitor-Induced Colitis: From Pathogenesis to Management.International journal of molecular sciences · 2023
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  19. Tafazzin deficiency in mouse mesenchymal stem cells promote reprogramming of activated B lymphocytes toward immunosuppressive phenotypes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
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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

13 authors at 3 institutions in 1 country.

Timo GaberDepartment of Rheumatology and Clinical Immunology, Charité⁻Universitätsmedizin Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, 10117 Berlin, Germany. timo.gaber@charite.de.
Kerstin SchönbeckDepartment of Rheumatology and Clinical Immunology, Charité⁻Universitätsmedizin Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, 10117 Berlin, Germany. kerstin.schoenbeck@charite.de.
Holger HoffGerman Rheumatism Research Centre (DRFZ) Berlin, A Leibniz Institute, 10117 Berlin, Germany. holger.hoff@icloud.com.
Cam Loan TranDepartment of Rheumatology and Clinical Immunology, Charité⁻Universitätsmedizin Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, 10117 Berlin, Germany. jinluan87@yahoo.de.
Cindy StrehlDepartment of Rheumatology and Clinical Immunology, Charité⁻Universitätsmedizin Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, 10117 Berlin, Germany. Strehl@drfz.de.
Annemarie LangDepartment of Rheumatology and Clinical Immunology, Charité⁻Universitätsmedizin Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, 10117 Berlin, Germany. annemarie.lang@charite.de.
Sarah OhrndorfDepartment of Rheumatology and Clinical Immunology, Charité⁻Universitätsmedizin Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, 10117 Berlin, Germany. sarah.ohrndorf@charite.de.
Moritz PfeiffenbergerDepartment of Rheumatology and Clinical Immunology, Charité⁻Universitätsmedizin Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, 10117 Berlin, Germany. moritz.pfeiffenberger@charite.de.
Eric RöhnerDepartment of Orthopedics, Campus Eisenberg, Jena University Hospital, Klosterlausnitzer Straße 81, 07607 Eisenberg, Germany. E.Roehner@krankenhaus-eisenberg.de.
Georg MatziolisDepartment of Orthopedics, Campus Eisenberg, Jena University Hospital, Klosterlausnitzer Straße 81, 07607 Eisenberg, Germany. G.Matziolis@krankenhaus-eisenberg.de.ORCID 0000-0002-5105-5875
Gerd-R BurmesterDepartment of Rheumatology and Clinical Immunology, Charité⁻Universitätsmedizin Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, 10117 Berlin, Germany. Gerd.Burmester@charite.de.
Frank ButtgereitDepartment of Rheumatology and Clinical Immunology, Charité⁻Universitätsmedizin Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, 10117 Berlin, Germany. Frank.Buttgereit@charite.de.
Paula HoffDepartment of Rheumatology and Clinical Immunology, Charité⁻Universitätsmedizin Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, 10117 Berlin, Germany. paula.hoff@charite.de.
Humboldt-Universität zu Berlin · DEJena University Hospital · DEGerman Rheumatism Research Centre · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mesenchymal stem/stromal cells (MSCs) are stem cells of the connective tissue, possess a plastic phenotype, and are able to differentiate into various tissues. Besides their role in tissue regeneration, MSCs perform additional functions as a modulator or inhibitor of immune responses. Due to their pleiotropic function, MSCs have also gained therapeutic importance for the treatment of autoimmune diseases and for improving fracture healing and cartilage regeneration. However, the therapeutic/immunomodulatory mode of action of MSCs is largely unknown. Here, we describe that MSCs express the inhibitory receptor CTLA-4 (cytotoxic T lymphocyte antigen 4). We show that depending on the environmental conditions, MSCs express different isoforms of CTLA-4 with the secreted isoform (sCTLA-4) being the most abundant under hypoxic conditions. Furthermore, we demonstrate that the immunosuppressive function of MSCs is mediated mainly by the secretion of CTLA-4. These findings open new ways for treatment when tissue regeneration/fracture healing is difficult.

Indexed as

AdipogenesisCells, CulturedCTLA-4 AntigenHumansImmune ToleranceMesenchymal Stem CellsOsteogenesisCTLA-4 AntigenCTLA4 protein, humanCTLA-4fracture healinghypoxiaimmune modulationmesenchymal stem/stromal cellsregeneration

Identifiers

PMID30087255
PMCPMC6121442
OpenAlexW2886040336

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.