Evidence map›Paper›PMID 30621275›Full record

ArticleCells2019

Assessment of the Immunosuppressive Potential of INF-γ Licensed Adipose Mesenchymal Stem Cells, Their Secretome and Extracellular Vesicles.

Teresa Raquel Tavares Serejo, Amandda Évelin Silva-Carvalho, Luma Dayane de Carvalho Filiú Braga, Francisco de Assis Rocha Neves, Rinaldo Wellerson Pereira, Juliana Lott de Carvalho, Felipe Saldanha-Araujo

Open access · goldAbstract read
In one paragraph

Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

49 citing papers in PubMed, 66 citations in OpenAlex.

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  14. IFN-Stem cells international · 2024
    Article
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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

7 authors at 2 institutions in 1 country.

Teresa Raquel Tavares SerejoLaboratório de Farmacologia Molecular, Departamento de Ciências da Saúde, Universidade de Brasília, Brasília 70910-900, Brazil. raquelserejo@yahoo.com.br.
Amandda Évelin Silva-CarvalhoLaboratório de Farmacologia Molecular, Departamento de Ciências da Saúde, Universidade de Brasília, Brasília 70910-900, Brazil. amanddaevelin@hotmail.com.
Luma Dayane de Carvalho Filiú BragaLaboratório de Farmacologia Molecular, Departamento de Ciências da Saúde, Universidade de Brasília, Brasília 70910-900, Brazil. luma.filiu@gmail.com.
Francisco de Assis Rocha NevesLaboratório de Farmacologia Molecular, Departamento de Ciências da Saúde, Universidade de Brasília, Brasília 70910-900, Brazil. nevesfar@gmail.com.
Rinaldo Wellerson PereiraPós-graduação em Ciências Genômicas e Biotecnologia, Universidade Católica de Brasília, Brasília 70790-160, Brazil. rinaldo.pereira@catolica.edu.br.
Juliana Lott de CarvalhoPós-graduação em Ciências Genômicas e Biotecnologia, Universidade Católica de Brasília, Brasília 70790-160, Brazil. julianalott@gmail.com.
Felipe Saldanha-AraujoLaboratório de Farmacologia Molecular, Departamento de Ciências da Saúde, Universidade de Brasília, Brasília 70910-900, Brazil. felipearaujo@unb.br.
Universidade de Brasília · BRUniversidade Católica de Brasília · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is an active search for the ideal strategy to potentialize the effects of Mesenchymal Stem-Cells (MSCs) over the immune system. Also, part of the scientific community is seeking to elucidate the therapeutic potential of MSCs secretome and its extracellular vesicles (EVs), in order to avoid the complexity of a cellular therapy. Here, we investigate the effects of human adipose MSCs (AMSCs) licensing with INF-γ and TLR3 agonist over AMSCs proliferation, migration, as well as the immunomodulatory function. Furthermore, we evaluated how the licensing of AMSCs affected the immunomodulatory function of AMSC derived-secretome, including their EVs. INF-γ licensed-AMSCs presented an elevated expression of indoleamine 2,3-dioxygenase (IDO), accompanied by increased ICAM-1, as well as a higher immunosuppressive potential, compared to unlicensed AMSCs. Interestingly, the conditioned medium obtained from INF-γ licensed-AMSCs also revealed a slightly superior immunosuppressive potential, compared to other licensing strategies. Therefore, unlicensed and INF-γ licensed-AMSCs groups were used to isolate EVs. Interestingly, EVs isolated from both groups displayed similar capacity to inhibit T-cell proliferation. EVs isolated from both groups shared similar TGF-β and Galectin-1 mRNA content but only EVs derived from INF-γ licensed-AMSCs expressed IDO mRNA. In summary, we demonstrated that INF-γ licensing of AMSCs provides an immunosuppressive advantage both from a cell-cell contact-dependent perspective, as well as in a cell-free context. Interestingly, EVs derived from unlicensed and INF-γ licensed-AMSCs have similar ability to control activated T-cell proliferation. These results contribute towards the development of new strategies to control the immune response based on AMSCs or their derived products.

Indexed as

Immune ToleranceAdipose TissueCell MovementCell ProliferationCells, CulturedCell SurvivalExtracellular VesiclesGalectin 1HumansIndoleamine-Pyrrole 2,3,-DioxygenaseIntercellular Adhesion Molecule-1Interferon-gammaMesenchymal Stem CellsToll-Like Receptor 3Transforming Growth Factor betaGalectin 1Indoleamine-Pyrrole 2,3,-DioxygenaseIntercellular Adhesion Molecule-1Interferon-gammaLGALS1 protein, humanTLR3 protein, humanToll-Like Receptor 3Transforming Growth Factor betaconditioned mediumextracellular vesiclesINF-γmesenchymal stem cellsT-cellsTLR

Identifiers

PMID30621275
PMCPMC6356584
OpenAlexW2907701151

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.