Evidence map›Paper›PMID 36630919›Full record

ArticleImmunity2023

Role of MR1-driven signals and amphiregulin on the recruitment and repair function of MAIT cells during skin wound healing.

Anastasia du Halgouet, Aurélie Darbois, Mansour Alkobtawi, Martin Mestdagh, Aurélia Alphonse, Virginie Premel, Thomas Yvorra, Ludovic Colombeau, Raphaël Rodriguez, Dietmar Zaiss and 8 more

Open access · hybridAbstract read
In one paragraph

Article in Immunity, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
13.3field-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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 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

18 authors at 3 institutions in 2 countries.

Anastasia du HalgouetINSERM U932, PSL University, Institut Curie, 75005 Paris, France.
Aurélie DarboisINSERM U932, PSL University, Institut Curie, 75005 Paris, France.
Mansour AlkobtawiCutaneous Biology, Institut Cochin, Inserm 1016, and Université de Paris Cité, 75014 Paris, France.
Martin MestdaghINSERM U932, PSL University, Institut Curie, 75005 Paris, France.
Aurélia AlphonseINSERM U932, PSL University, Institut Curie, 75005 Paris, France.
Virginie PremelINSERM U932, PSL University, Institut Curie, 75005 Paris, France.
Thomas YvorraCNRS UMR 3666, INSERM U1143, Chemical Biology of Cancer Laboratory, PSL University, Institut Curie, 75005 Paris, France.
Ludovic ColombeauCNRS UMR 3666, INSERM U1143, Chemical Biology of Cancer Laboratory, PSL University, Institut Curie, 75005 Paris, France.
Raphaël RodriguezCNRS UMR 3666, INSERM U1143, Chemical Biology of Cancer Laboratory, PSL University, Institut Curie, 75005 Paris, France.
Dietmar ZaissDepartment of Immune Medicine, University of Regensburg, Regensburg, Germany; Institute of Clinical Chemistry and Laboratory Medicine, University Hospital Regensburg, Regensburg, Germany; Institute of Pathology, University Regensburg, Regensburg, Germany; Leibniz Institute for Immunotherapy (LIT), Regensburg, Germany.
Yara El MorrINSERM U932, PSL University, Institut Curie, 75005 Paris, France.
Hélène BugautINSERM U932, PSL University, Institut Curie, 75005 Paris, France.
François LegouxINSERM U932, PSL University, Institut Curie, 75005 Paris, France.
Laetitia PerrinINSERM U932, PSL University, Institut Curie, 75005 Paris, France.
Selim AractingiCutaneous Biology, Institut Cochin, Inserm 1016, and Université de Paris Cité, 75014 Paris, France.
Rachel GolubInstitut Pasteur, Université Paris Cité, INSERM U1223, 75015 Paris, France.
Olivier LantzINSERM U932, PSL University, Institut Curie, 75005 Paris, France; Laboratoire d'Immunologie Clinique, Institut Curie, 75005 Paris, France; Centre d'investigation Clinique en Biothérapie Gustave-Roussy Institut Curie (CIC-BT1428), Institut Curie, 75005 Paris, France. Electronic address: olivier.lantz@curie.fr.
Marion SalouINSERM U932, PSL University, Institut Curie, 75005 Paris, France. Electronic address: marion.salou@curie.fr.
Inserm · FRCentre National de la Recherche Scientifique · FRUniversity Hospital Regensburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tissue repair processes maintain proper organ function following mechanical or infection-related damage. In addition to antibacterial properties, mucosal associated invariant T (MAIT) cells express a tissue repair transcriptomic program and promote skin wound healing when expanded. Herein, we use a human-like mouse model of full-thickness skin excision to assess the underlying mechanisms of MAIT cell tissue repair function. Single-cell RNA sequencing analysis suggested that skin MAIT cells already express a repair program at steady state. Following skin excision, MAIT cells promoted keratinocyte proliferation, thereby accelerating healing. Using skin grafts, parabiosis, and adoptive transfer experiments, we show that MAIT cells migrated into the wound in a T cell receptor (TCR)-independent but CXCR6 chemokine receptor-dependent manner. Amphiregulin secreted by MAIT cells following excision promoted wound healing. Expression of the repair function was probably independent of sustained TCR stimulation. Overall, our study provides mechanistic insights into MAIT cell wound healing function in the skin.

Indexed as

AmphiregulinHistocompatibility Antigens Class IMucosal-Associated Invariant T CellsWound HealingAnimalsHumansMiceMinor Histocompatibility AntigensReceptors, Antigen, T-CellAmphiregulinHistocompatibility Antigens Class IMinor Histocompatibility AntigensMR1 protein, humanMr1 protein, mouseReceptors, Antigen, T-CellamphiregulinCXCR6 chemokine receptorMAIT cellsscRNA-seqskin excisionTCR signalingtissue repair

Identifiers

PMID36630919
PMCPMC9839364
OpenAlexW4314937975

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.