Evidence map›Paper›PMID 31001285›Full record

ArticleFrontiers in immunology2019

Activated Mesenchymal Stromal Cells Process and Present Antigens Regulating Adaptive Immunity.

Kayleigh M van Megen, Ernst-Jan T van 't Wout, Julia Lages Motta, Bernice Dekker, Tatjana Nikolic, Bart O Roep

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

55 citing papers in PubMed, 79 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

6 authors at 3 institutions in 3 countries.

Kayleigh M van MegenDepartment of Diabetes Immunology, Diabetes and Metabolism Research Institute at the Beckman Research Institute of City of Hope, Duarte, CA, United States.
Ernst-Jan T van 't WoutDepartment of Diabetes Immunology, Diabetes and Metabolism Research Institute at the Beckman Research Institute of City of Hope, Duarte, CA, United States.
Julia Lages MottaDepartment of Immunohaematology and Blood Transfusion, Leiden University Medical Center, Leiden, Netherlands.
Bernice DekkerDepartment of Immunohaematology and Blood Transfusion, Leiden University Medical Center, Leiden, Netherlands.
Tatjana NikolicDepartment of Immunohaematology and Blood Transfusion, Leiden University Medical Center, Leiden, Netherlands.
Bart O RoepDepartment of Diabetes Immunology, Diabetes and Metabolism Research Institute at the Beckman Research Institute of City of Hope, Duarte, CA, United States.
Leiden University Medical Center · NLCity of Hope · USUniversidade Federal de Minas Gerais · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mesenchymal stromal cells (MSCs) are inherently immunomodulatory through production of inhibiting soluble factors and expression of immunosuppressive cell surface markers. We tested whether activated MSCs qualify for the induction of antigen-specific immune regulation. Bone marrow derived human MSCs were activated by interferon-γ and analyzed for antigen uptake and processing and immune regulatory features including phenotype, immunosuppressive capacity, and metabolic activity. To assess whether activated MSC can modulate adaptive immunity, MSCs were pulsed with islet auto-antigen (GAD65) peptide to stimulate GAD65-specific T-cells. We confirm that inflammatory activation of MSCs increased HLA class II, PD-L1, and intracellular IDO expression, whereas co-stimulatory molecules including CD86 remained absent. MSCs remained locked in their metabolic phenotype, as activation did not alter glycolytic function or mitochondrial respiration. MSCs were able to uptake and process protein. Activated HLA-DR3-expressing MSCs pulsed with GAD65 peptide inhibited proliferation of HLA-DR3-restricted GAD65-specific T-cells, while this HLA class II expression did not induce cellular alloreactivity. Conditioning of antigen-specific T-cells by activated and antigen-pulsed MSCs prevented T-cells to proliferate upon subsequent activation by dendritic cells, even after removal of the MSCs. In sum, activation of MSCs with inflammatory stimuli turns these cells into suppressive cells capable of mediating adaptive regulation of proinflammatory pathogenic T-cells.

Indexed as

Antigen PresentationAutoantigensB7-2 AntigenGlutamate DecarboxylaseHistocompatibility Antigens Class IIHumansMesenchymal Stem CellsT-LymphocytesAutoantigensB7-2 AntigenCD86 protein, humanGlutamate DecarboxylaseHistocompatibility Antigens Class IIantigen presenting cell (APC)antigen specificimmune regulationimmunotherapymesenchymal stromal cell (MSC)type 1 diabetes (T1D)

Identifiers

PMID31001285
PMCPMC6457321
OpenAlexW2925828015

What OpenQuestion holds

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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.