Evidence map›Paper›PMID 29629900›Full record

ArticleThe Journal of clinical investigation2018

Recipient mucosal-associated invariant T cells control GVHD within the colon.

Antiopi Varelias, Mark D Bunting, Kate L Ormerod, Motoko Koyama, Stuart D Olver, Jasmin Straube, Rachel D Kuns, Renee J Robb, Andrea S Henden, Leanne Cooper and 12 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 1 pooled it
5.6field-weighted citation impact, top 3% 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

71 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  6. Article
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  8. Article
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  10. Gut microbiota and acute graft-versus-host disease.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2025
    Article
  11. Review
  12. Review
  13. Article
  14. MAIT cells modulating the oral lichen planus immune microenvironment: a cellular crosstalk perspective.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  15. MAIT cells: Conserved watchers on the wall.The Journal of experimental medicine · 2025
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

11 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

22 authors at 6 institutions in 4 countries.

Antiopi VareliasBone Marrow Transplantation Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, Australia.
Mark D BuntingBone Marrow Transplantation Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, Australia.
Kate L OrmerodAustralian Centre for Ecogenomics, The University of Queensland, Brisbane, Australia.
Motoko KoyamaBone Marrow Transplantation Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, Australia.
Stuart D OlverBone Marrow Transplantation Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, Australia.
Jasmin StraubeGordon and Jessie Gilmour Leukaemia Research Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, Australia.
Rachel D KunsBone Marrow Transplantation Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, Australia.
Renee J RobbBone Marrow Transplantation Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, Australia.
Andrea S HendenBone Marrow Transplantation Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, Australia.
Leanne CooperGordon and Jessie Gilmour Leukaemia Research Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, Australia.
Nancy LachnerAustralian Centre for Ecogenomics, The University of Queensland, Brisbane, Australia.
Kate H GartlanBone Marrow Transplantation Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, Australia.
Olivier LantzINSERM U932 and Department de Biologie des Tumeurs, Institute Curie and Centre d'Investigation Clinique, CICBT507 IGR/Curie, Paris, France.
Lars Kjer-NielsenDepartment of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, University of Melbourne, Parkville, Australia.
Jeffrey Yw MakAustralian Research Council Centre of Excellence in Advanced Molecular Imaging, Institute for Molecular Bioscience, The University of Queensland, Brisbane, Australia.
David P FairlieAustralian Research Council Centre of Excellence in Advanced Molecular Imaging, Institute for Molecular Bioscience, The University of Queensland, Brisbane, Australia.
Andrew D CloustonEnvoi Specialist Pathologists, Brisbane, Australia.
James McCluskeyDepartment of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, University of Melbourne, Parkville, Australia.
Jamie RossjohnInfection and Immunity Program and The Department of Biochemistry and Molecular Biology, Biomedicine Discovery Institute Monash University, Clayton, Australia.
Steven W LaneFaculty of Medicine, and.
Philip HugenholtzAustralian Centre for Ecogenomics, The University of Queensland, Brisbane, Australia.
Geoffrey R HillBone Marrow Transplantation Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, Australia.
QIMR Berghofer Medical Research Institute · AUAustralian Research Council · AUThe University of Queensland · AUThe University of Melbourne · AUEnvoi Specialist Pathologists · AUInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mucosal-associated invariant T (MAIT) cells are a unique innate-like T cell subset that responds to a wide array of bacteria and yeast through recognition of riboflavin metabolites presented by the MHC class I-like molecule MR1. Here, we demonstrate using MR1 tetramers that recipient MAIT cells are present in small but definable numbers in graft-versus-host disease (GVHD) target organs and protect from acute GVHD in the colon following bone marrow transplantation (BMT). Consistent with their preferential juxtaposition to microbial signals in the colon, recipient MAIT cells generate large amounts of IL-17A, promote gastrointestinal tract integrity, and limit the donor alloantigen presentation that in turn drives donor Th1 and Th17 expansion specifically in the colon after BMT. Allogeneic BMT recipients deficient in IL-17A also develop accelerated GVHD, suggesting MAIT cells likely regulate GVHD, at least in part, by the generation of this cytokine. Indeed, analysis of stool microbiota and colon tissue from IL-17A-/- and MR1-/- mice identified analogous shifts in microbiome operational taxonomic units (OTU) and mediators of barrier integrity that appear to represent pathways controlled by similar, IL-17A-dependent mechanisms. Thus, MAIT cells act to control barrier function to attenuate pathogenic T cell responses in the colon and, given their very high frequency in humans, likely represent an important population in clinical BMT.

Indexed as

Bone Marrow TransplantationAllograftsAnimalsColonColonic DiseasesFemaleGraft vs Host DiseaseMiceMice, Inbred BALB CMice, KnockoutMucosal-Associated Invariant T CellsTh17 CellsBone marrow transplantationImmunologyTransplantation

Identifiers

PMID29629900
PMCPMC5919881
OpenAlexW2796163301

What OpenQuestion holds

Textmetadata
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.