Evidence map›Paper›PMID 26063000›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2015

Functional Heterogeneity and Antimycobacterial Effects of Mouse Mucosal-Associated Invariant T Cells Specific for Riboflavin Metabolites.

Isaac G Sakala, Lars Kjer-Nielsen, Christopher S Eickhoff, Xiaoli Wang, Azra Blazevic, Ligong Liu, David P Fairlie, Jamie Rossjohn, James McCluskey, Daved H Fremont and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 1 pooled it
6.9field-weighted citation impact, top 2% 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

79 citing papers in PubMed, 1 synthesis or guideline pooled it, 132 citations in OpenAlex.

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19 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

12 authors at 7 institutions in 5 countries.

Isaac G SakalaDivision of Infectious Diseases, Allergy, and Immunology, Department of Internal Medicine, Saint Louis University School of Medicine, Saint Louis, MO 63104; Department of Pathology and Immunology, Washington University School of Medicine, Saint Louis, MO 63110; hoftdf@slu.edu hansen@pathology.wustl.edu isaac.sakala@gmail.com.
Lars Kjer-NielsenDepartment of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, University of Melbourne, Parkville, Victoria 3010, Australia;
Christopher S EickhoffDivision of Infectious Diseases, Allergy, and Immunology, Department of Internal Medicine, Saint Louis University School of Medicine, Saint Louis, MO 63104;
Xiaoli WangDepartment of Pathology and Immunology, Washington University School of Medicine, Saint Louis, MO 63110;
Azra BlazevicDivision of Infectious Diseases, Allergy, and Immunology, Department of Internal Medicine, Saint Louis University School of Medicine, Saint Louis, MO 63104;
Ligong LiuDivision of Chemistry and Structural Biology, Institute of Molecular Bioscience, University of Queensland, Brisbane, Queensland 4072, Australia; Australian Research Council Centre of Excellence in Advanced Molecular Imaging, University of Queensland, Brisbane, Queensland 4072, Australia;
David P FairlieDivision of Chemistry and Structural Biology, Institute of Molecular Bioscience, University of Queensland, Brisbane, Queensland 4072, Australia; Australian Research Council Centre of Excellence in Advanced Molecular Imaging, University of Queensland, Brisbane, Queensland 4072, Australia;
Jamie RossjohnDepartment of Biochemistry and Molecular Biology, School of Biomedical Sciences, Monash University, Clayton, Melbourne, Victoria 3800 Australia; Institute of Infection and Immunity, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, United Kingdom; Australian Research Council Centre of Excellence for Advanced Molecular Imaging, Monash University, Clayton, Victoria 3800, Australia; and.
James McCluskeyDepartment of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, University of Melbourne, Parkville, Victoria 3010, Australia;
Daved H FremontDepartment of Pathology and Immunology, Washington University School of Medicine, Saint Louis, MO 63110;
Ted H HansenDepartment of Pathology and Immunology, Washington University School of Medicine, Saint Louis, MO 63110; hoftdf@slu.edu hansen@pathology.wustl.edu isaac.sakala@gmail.com.
Daniel F HoftDivision of Infectious Diseases, Allergy, and Immunology, Department of Internal Medicine, Saint Louis University School of Medicine, Saint Louis, MO 63104; Department of Microbiology and Immunology, Edward A. Doisy Research Center, Saint Louis University School of Medicine, Saint Louis, MO 63104 hoftdf@slu.edu hansen@pathology.wustl.edu isaac.sakala@gmail.com.
Saint Louis University · USWashington University in St. Louis · USUniversity of Queensland · AUInstitute of Infection and Immunity · CAPeter Doherty Institute · AUSaint Louis University · ESUniversity of Melbourne · AU

Funding

Role of gammadelta T Cells in Vaccine-Induced ImmunityR01AI048391 · NIAID · SAINT LOUIS UNIVERSITY · PI HOFT, DANIEL F. · 2002 to 2019
$6.1M
MR1 BIOCHEMICAL FEATURES AND IMMUNOLOGICAL FUNCTIONSR01AI046553 · NIAID · WASHINGTON UNIVERSITY · PI FREMONT, DAVED H., HOFT, DANIEL F. · 2000 to 2014
$4.6M
NIAID NIH HHS R01 AI046553NIAID NIH HHS R01-AI046553NIAID NIH HHS R01 AI048391PHS HHS R01-A148391
6 · The paper itself

Abstract

Mucosal-associated invariant T (MAIT) cells have a semi-invariant TCR Vα-chain, and their optimal development is dependent upon commensal flora and expression of the nonpolymorphic MHC class I-like molecule MR1. MAIT cells are activated in an MR1-restricted manner by diverse strains of bacteria and yeast, suggesting a widely shared Ag. Recently, human and mouse MR1 were found to bind bacterial riboflavin metabolites (ribityllumazine [RL] Ags) capable of activating MAIT cells. In this study, we used MR1/RL tetramers to study MR1 dependency, subset heterogeneity, and protective effector functions important for tuberculosis immunity. Although tetramer(+) cells were detected in both MR1(+/+) and MR1(-/-) TCR Vα19i-transgenic (Tg) mice, MR1 expression resulted in significantly increased tetramer(+) cells coexpressing TCR Vβ6/8, NK1.1, CD44, and CD69 that displayed more robust in vitro responses to IL-12 plus IL-18 and RL Ag, indicating that MR1 is necessary for the optimal development of the classic murine MAIT cell memory/effector subset. In addition, tetramer(+) MAIT cells expressing CD4, CD8, or neither developing in MR1(+/+) Vα19i-Tg mice had disparate cytokine profiles in response to RL Ag. Therefore, murine MAIT cells are considerably more heterogeneous than previously thought. Most notably, after mycobacterial pulmonary infection, heterogeneous subsets of tetramer(+) Vα19i-Tg MAIT cells expressing CXCR3 and α4β1 were recruited into the lungs and afforded early protection. In addition, Vα19iCα(-/-)MR(+/+) mice were significantly better protected than were Vα19iCα(-/-)MR1(-/-), wild-type, and MR1(-/-) non-Tg mice. Overall, we demonstrate considerable functional diversity of MAIT cell responses, as well as that MR1-restricted MAIT cells are important for tuberculosis protective immunity.

Indexed as

Immunity, MucosalAnimalsAntigens, CDAntigens, Differentiation, T-LymphocyteAntigens, LyCD4-Positive T-LymphocytesCD69 AntigensCD8-Positive T-LymphocytesCells, CulturedGene Expression Regulation, DevelopmentalGenetic HeterogeneityHistocompatibility Antigens Class IHyaluronan ReceptorsImmunologic MemoryIntegrin alpha4beta1Interleukin-12Antigens, CDAntigens, Differentiation, T-LymphocyteAntigens, LyCd44 protein, mouseCD69 AntigensCxcr3 protein, mouseHistocompatibility Antigens Class IHyaluronan ReceptorsIntegrin alpha4beta1Interleukin-12Interleukin-18Klrb1c protein, mouseLectins, C-TypeMinor Histocompatibility AntigensMr1 protein, mouseNK Cell Lectin-Like Receptor Subfamily BReceptors, Antigen, T-Cell, alpha-betaReceptors, CXCR3Riboflavin

Identifiers

PMID26063000
PMCPMC4490942
OpenAlexW1819166087

What OpenQuestion holds

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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.