Evidence map›Paper›PMID 29858567›Full record

ArticleNature communications2018

Mucosal-associated invariant T cells are a profibrogenic immune cell population in the liver.

Pushpa Hegde, Emmanuel Weiss, Valérie Paradis, Jinghong Wan, Morgane Mabire, Sukriti Sukriti, Pierre-Emmanuel Rautou, Miguel Albuquerque, Olivia Picq, Abhishak Chandra Gupta and 9 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers.

0numbers the graph read from it
0cells of the map it votes in
130citing papers in PubMed
9.2field-weighted citation impact, top 1% 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

130 citing papers in PubMed, 216 citations in OpenAlex.

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  20. Inflammation in MASLD progression and cancer.JHEP reports : innovation in hepatology · 2025
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70 more citing papers are in PubMed but not listed here.

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

19 authors at 3 institutions in 1 country.

Pushpa HegdeInserm UMR-1149, Centre de Recherche sur l'Inflammation, 75018, Paris, France.
Emmanuel WeissInserm UMR-1149, Centre de Recherche sur l'Inflammation, 75018, Paris, France.
Valérie ParadisInserm UMR-1149, Centre de Recherche sur l'Inflammation, 75018, Paris, France.
Jinghong WanInserm UMR-1149, Centre de Recherche sur l'Inflammation, 75018, Paris, France.
Morgane MabireInserm UMR-1149, Centre de Recherche sur l'Inflammation, 75018, Paris, France.
Sukriti SukritiInserm UMR-1149, Centre de Recherche sur l'Inflammation, 75018, Paris, France.
Pierre-Emmanuel RautouDépartement Hospitalo-Universitaire (DHU) UNITY, Service d'Hépatologie, Hôpital Beaujon, Assistance Publique-Hôpitaux de Paris, 92110, Clichy, France.
Miguel AlbuquerqueInserm UMR-1149, Centre de Recherche sur l'Inflammation, 75018, Paris, France.
Olivia PicqInserm UMR-1149, Centre de Recherche sur l'Inflammation, 75018, Paris, France.
Abhishak Chandra GuptaInserm UMR-1149, Centre de Recherche sur l'Inflammation, 75018, Paris, France.
Gladys FerrereInserm UMR-1149, Centre de Recherche sur l'Inflammation, 75018, Paris, France.
Hélène GilgenkrantzInserm UMR-1149, Centre de Recherche sur l'Inflammation, 75018, Paris, France.
Badr KiafInserm U-1016, CNRS UMR 8104, Institut Cochin, Université Paris-Descartes, 75014, Paris, France.
Amine ToubalInserm U-1016, CNRS UMR 8104, Institut Cochin, Université Paris-Descartes, 75014, Paris, France.
Lucie BeaudoinInserm U-1016, CNRS UMR 8104, Institut Cochin, Université Paris-Descartes, 75014, Paris, France.
Philippe LettéronInserm UMR-1149, Centre de Recherche sur l'Inflammation, 75018, Paris, France.
Richard MoreauInserm UMR-1149, Centre de Recherche sur l'Inflammation, 75018, Paris, France.ORCID http://orcid.org/0000-0003-0862-403X
Agnès LehuenInserm U-1016, CNRS UMR 8104, Institut Cochin, Université Paris-Descartes, 75014, Paris, France. agnes.lehuen@inserm.fr.ORCID http://orcid.org/0000-0002-0450-3321
Sophie LotersztajnInserm UMR-1149, Centre de Recherche sur l'Inflammation, 75018, Paris, France. sophie.lotersztajn@inserm.fr.
Inserm · FRCentre National de la Recherche Scientifique · FRHôpital Beaujon · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver fibrosis is the common response to chronic liver injury, and leads to cirrhosis and its complications. Persistent inflammation is a driving force of liver fibrosis progression. Mucosal-associated invariant T (MAIT) cells are non-conventional T cells that display altered functions during chronic inflammatory diseases. Here, we show that circulating MAIT cells are reduced in patients with alcoholic or non-alcoholic fatty liver disease-related cirrhosis while they accumulate in liver fibrotic septa. Using two models of chronic liver injury, we demonstrate that MAIT cell-enriched mice show increased liver fibrosis and accumulation of hepatic fibrogenic cells, whereas MAIT cell-deficient mice are resistant. Co-culture experiments indicate that MAIT cells enhance the proinflammatory properties of monocyte-derived macrophages, and promote mitogenic and proinflammatory functions of fibrogenic cells, via distinct mechanisms. Our results highlight the profibrogenic functions of MAIT cells and suggest that targeting MAIT cells may constitute an attractive antifibrogenic strategy during chronic liver injury.

Indexed as

AdultAgedAnimalsCell CountCells, CulturedCoculture TechniquesFemaleHumansLiverLiver CirrhosisMacrophagesMaleMiceMiddle AgedMucosal-Associated Invariant T CellsNon-alcoholic Fatty Liver Disease

Identifiers

PMID29858567
PMCPMC5984626
OpenAlexW2807359581

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.