Evidence map›Paper›PMID 32106283›Full record

ArticleThe Journal of experimental medicine2020

A population of proinflammatory T cells coexpresses αβ and γδ T cell receptors in mice and humans.

Sarah C Edwards, Caroline E Sutton, Kristin Ladell, Emma J Grant, James E McLaren, Fiona Roche, Pradyot Dash, Nopporn Apiwattanakul, Walid Awad, Kelly L Miners and 17 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

33 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
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  12. Article
  13. γδ T cells: origin and fate, subsets, diseases and immunotherapy.Signal transduction and targeted therapy · 2023
    Review
  14. Review
  15. Steady-state memory-phenotype conventional CD4Experimental & molecular medicine · 2023
    Article
  16. Review
  17. Article
  18. Review
  19. Cell reports methods · 2022
    Article
  20. Review
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

27 authors at 7 institutions in 6 countries.

Sarah C EdwardsImmune Regulation Research Group, School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland.
Caroline E SuttonImmune Regulation Research Group, School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland.
Kristin LadellDivision of Infection and Immunity, Cardiff University School of Medicine, Heath Park, Cardiff, UK.
Emma J GrantDivision of Infection and Immunity, Cardiff University School of Medicine, Heath Park, Cardiff, UK.
James E McLarenDivision of Infection and Immunity, Cardiff University School of Medicine, Heath Park, Cardiff, UK.
Fiona RocheSmurfit Institute of Genetics, Trinity College Dublin, Dublin, Ireland.
Pradyot DashDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN.
Nopporn ApiwattanakulDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN.
Walid AwadDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN.
Kelly L MinersDivision of Infection and Immunity, Cardiff University School of Medicine, Heath Park, Cardiff, UK.
Stephen J LalorHost Pathogen Interactions Group, School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland.
Julie C RibotInstituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal.
Song BaikInstitute of Immunology and Immunotherapy, College of Medical and Dental Sciences, Medical School, University of Birmingham, Edgbaston, Birmingham, UK.
Barry MoranImmune Regulation Research Group, School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland.
Aoife McGinleyImmune Regulation Research Group, School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland.
Valerie PivorunasAbbVie Bioresearch Center, Inc., Worcester, MA.
Lori DowdingAbbVie Bioresearch Center, Inc., Worcester, MA.
Michael MacorittoAbbVie Bioresearch Center, Inc., Worcester, MA.
Jesus Paez-CortezAbbVie Bioresearch Center, Inc., Worcester, MA.
Anthony SlavinAbbVie Bioresearch Center, Inc., Worcester, MA.
Graham AndersonInstitute of Immunology and Immunotherapy, College of Medical and Dental Sciences, Medical School, University of Birmingham, Edgbaston, Birmingham, UK.
Bruno Silva-SantosInstituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal.
Karsten HokampSmurfit Institute of Genetics, Trinity College Dublin, Dublin, Ireland.
David A PriceDivision of Infection and Immunity, Cardiff University School of Medicine, Heath Park, Cardiff, UK.
Paul G ThomasDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN.
Rachel M McLoughlinHost Pathogen Interactions Group, School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland.
Kingston H G MillsImmune Regulation Research Group, School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland.
Trinity College Dublin · IEAbbVie (United States) · USSt. Jude Children's Research Hospital · USCardiff University · GBUniversity of Birmingham · GBUniversity of Lisbon · PTAustralian Regenerative Medicine Institute · AU

Funding

Mechanisms to diversify repertoire and modify T cell activity after infectionR01AI107625 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI THOMAS, PAUL G. · 2013 to 2017
$2.3M
Medical Research Council G1000213NIAID NIH HHS R01 AI107625Wellcome TrustWellcome Trust 100326Z/12/Z
6 · The paper itself

Abstract

T cells are classically recognized as distinct subsets that express αβ or γδ TCRs. We identify a novel population of T cells that coexpress αβ and γδ TCRs in mice and humans. These hybrid αβ-γδ T cells arose in the murine fetal thymus by day 16 of ontogeny, underwent αβ TCR-mediated positive selection into CD4+ or CD8+ thymocytes, and constituted up to 10% of TCRδ+ cells in lymphoid organs. They expressed high levels of IL-1R1 and IL-23R and secreted IFN-γ, IL-17, and GM-CSF in response to canonically restricted peptide antigens or stimulation with IL-1β and IL-23. Hybrid αβ-γδ T cells were transcriptomically distinct from conventional γδ T cells and displayed a hyperinflammatory phenotype enriched for chemokine receptors and homing molecules that facilitate migration to sites of inflammation. These proinflammatory T cells promoted bacterial clearance after infection with Staphylococcus aureus and, by licensing encephalitogenic Th17 cells, played a key role in the development of autoimmune disease in the central nervous system.

Indexed as

AnimalsBiomarkersEncephalomyelitis, Autoimmune, ExperimentalHumansInflammationLymphocyte ActivationMice, Inbred C57BLPhenotypeReceptors, Antigen, T-Cell, alpha-betaReceptors, Antigen, T-Cell, gamma-deltaStaphylococcal InfectionsStaphylococcus aureusT-LymphocytesTranscription, GeneticTranscriptomeBiomarkersReceptors, Antigen, T-Cell, alpha-betaReceptors, Antigen, T-Cell, gamma-delta

Identifiers

PMID32106283
PMCPMC7201916
OpenAlexW3007464489

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.