Evidence map›Paper›PMID 37516912›Full record

ArticleThe Journal of experimental medicine2023

Type I interferons drive MAIT cell functions against bacterial pneumonia.

Juan Carlos López-Rodríguez, Steven J Hancock, Kelin Li, Stefania Crotta, Christopher Barrington, Alejandro Suárez-Bonnet, Simon L Priestnall, Jeffrey Aubé, Andreas Wack, Paul Klenerman and 2 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

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  12. TET3 is expressed in prostate cancer tumor-associated macrophages and is associated with anti-androgen resistance.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
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  14. MAIT cells: Conserved watchers on the wall.The Journal of experimental medicine · 2025
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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

12 authors at 6 institutions in 2 countries.

Juan Carlos López-RodríguezThe Peter Gorer Department of Immunobiology, King's College London, London, UK.ORCID 0000-0002-6106-6551
Steven J HancockWellcome-Wolfson Institute for Experimental Medicine. School of Medicine, Dentistry and Biomedical Sciences, Queen's University Belfast , Belfast, UK.ORCID 0000-0001-7203-2640
Kelin LiDivision of Chemical Biology and Medicinal Chemistry, UNC Eshelman School of Pharmacy, University of North Carolina at Chapel Hill , Chapel Hill, NC, USA.ORCID 0000-0002-8630-2928
Stefania CrottaThe Francis Crick Institute , London, UK.ORCID 0000-0003-4676-8616
Christopher BarringtonThe Francis Crick Institute , London, UK.ORCID 0000-0003-1281-2658
Alejandro Suárez-BonnetThe Francis Crick Institute , London, UK.ORCID 0000-0003-0296-5896
Simon L PriestnallThe Francis Crick Institute , London, UK.ORCID 0000-0002-6027-1879
Jeffrey AubéDivision of Chemical Biology and Medicinal Chemistry, UNC Eshelman School of Pharmacy, University of North Carolina at Chapel Hill , Chapel Hill, NC, USA.ORCID 0000-0003-1049-5767
Andreas WackThe Francis Crick Institute , London, UK.ORCID 0000-0001-5226-2991
Paul KlenermanPeter Medawar Building for Pathogen Research , Oxford, UK.ORCID 0000-0003-4307-9161
Jose A BengoecheaWellcome-Wolfson Institute for Experimental Medicine. School of Medicine, Dentistry and Biomedical Sciences, Queen's University Belfast , Belfast, UK.ORCID 0000-0002-9677-8751
Patricia BarralThe Peter Gorer Department of Immunobiology, King's College London, London, UK.ORCID 0000-0003-4324-8973
The Francis Crick Institute · GBKing's College London · GBQueen's University Belfast · GBRoyal Veterinary College · GBUniversity of North Carolina at Chapel Hill · USMedawar Building for Pathogen Research · GB

Funding

Virology Research Program (Program 4)P30CA016086 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI David Darr · 1985 to 2026
$201.5M
Biotechnology and Biological Sciences Research Council BB/S005560/1Medical Research Council MC_U117597139NCI NIH HHS P30 CA016086
6 · The paper itself

Abstract

Mucosal-associated invariant T (MAIT) cells are abundant in the lung and contribute to host defense against infections. During bacterial infections, MAIT cell activation has been proposed to require T cell receptor (TCR)-mediated recognition of antigens derived from the riboflavin synthesis pathway presented by the antigen-presenting molecule MR1. MAIT cells can also be activated by cytokines in an MR1-independent manner, yet the contribution of MR1-dependent vs. -independent signals to MAIT cell functions in vivo remains unclear. Here, we use Klebsiella pneumoniae as a model of bacterial pneumonia and demonstrate that MAIT cell activation is independent of MR1 and primarily driven by type I interferons (IFNs). During Klebsiella infection, type I IFNs stimulate activation of murine and human MAIT cells, induce a Th1/cytotoxic transcriptional program, and modulate MAIT cell location within the lungs. Consequently, adoptive transfer or boosting of pulmonary MAIT cells protect mice from Klebsiella infection, with protection being dependent on direct type I IFN signaling on MAIT cells. These findings reveal type I IFNs as new molecular targets to manipulate MAIT cell functions during bacterial infections.

Indexed as

Interferon Type IKlebsiella InfectionsMucosal-Associated Invariant T CellsPneumonia, BacterialAnimalsHumansKlebsiella pneumoniaeMiceInterferon Type I

Identifiers

PMID37516912
PMCPMC10373297
OpenAlexW4385387052

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.