Evidence map›Paper›PMID 25786692›Full record

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

The TNF-family ligand TL1A and its receptor DR3 promote T cell-mediated allergic immunopathology by enhancing differentiation and pathogenicity of IL-9-producing T cells.

Arianne C Richard, Cuiyan Tan, Eric T Hawley, Julio Gomez-Rodriguez, Ritobrata Goswami, Xiang-Ping Yang, Anthony C Cruz, Pallavi Penumetcha, Erika T Hayes, Martin Pelletier and 11 more

Erratum issuedOpen 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. An erratum has been issued. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

67 citing papers in PubMed, 116 citations in OpenAlex.

  1. Review
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  13. The World according to IL-9.Journal of immunology (Baltimore, Md. : 1950) · 2023
    Article
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7 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

21 authors at 5 institutions in 2 countries.

Arianne C RichardImmunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892;
Cuiyan TanExperimental Immunology Section, National Eye Institute, National Institutes of Health, Bethesda, MD 20892;
Eric T HawleyImmunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892;
Julio Gomez-RodriguezGenetic Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892;
Ritobrata GoswamiDepartment of Pediatrics and Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN 46202;
Xiang-Ping YangMolecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892;
Anthony C CruzImmunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892;
Pallavi PenumetchaImmunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892;
Erika T HayesImmunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892;
Martin PelletierImmunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892;
Odile GabayImmunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892;
Matthew WalshDepartment of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA 19102;
John R FerdinandImmunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892; Cancer Sciences Academic Unit, Faculty of Medicine, University of Southampton, Southampton SO17 1BJ, United Kingdom; and.
Andrea Keane-MyersBiological Defense Research Directorate, Naval Medical Research Center-Frederick, Fort Detrick, MD 21702.
Yongwon ChoiDepartment of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA 19102;
John J O'SheaMolecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892;
Aymen Al-ShamkhaniCancer Sciences Academic Unit, Faculty of Medicine, University of Southampton, Southampton SO17 1BJ, United Kingdom; and.
Mark H KaplanDepartment of Pediatrics and Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN 46202;ORCID http://orcid.org/0000-0002-2923-8245
Igal GeryExperimental Immunology Section, National Eye Institute, National Institutes of Health, Bethesda, MD 20892;
Richard M SiegelImmunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892; rsiegel@nih.gov.
Françoise MeylanImmunoregulation Section, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892;
National Institutes of Health · USIndiana University – Purdue University Indianapolis · USUniversity of Pennsylvania · USNaval Medical Research Command · USUniversity of Southampton · GB

Funding

Stat transcription factors in immunoregulation and autoimmune diseaseZIAAR041159 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI O'SHEA, JOHN · 2009 to 2025
$49.3M
Genetic and Biochemical Approaches to Tyrosine Kinase FunctionZIAHG000123 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI SCHWARTZBERG, PAMELA · 2009 to 2018
$20.8M
TL1A and its receptor DR3 in normal and autoimmune T cell responsesZIAAR041174 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI SIEGEL, RICHARD M · 2009 to 2019
$9.8M
Immune Responses To Ocular AntigensZIAEY000069 · NEI · NATIONAL EYE INSTITUTE · PI GERY, IGAL · 2009 to 2017
$9.2M
The role of PU.1 in T helper cell heterogeneityR01AI057459 · NIAID · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI KAPLAN, MARK H · 2005 to 2025
$8.2M
Indiana Medical Scientist/Engineer Training ProgramT32GM077229 · NIGMS · INDIANA UNIVERSITY INDIANAPOLIS · PI GASTON, BENJAMIN, HERBERT, BRITTNEY-SHEA · 2008 to 2022
$6.0M
Cancer Research UK 13211Cancer Research UK 19502Intramural NIH HHS ZIA AR041174NIAID NIH HHS R01 AI057459NIGMS NIH HHS T32 GM077229Wellcome Trust
6 · The paper itself

Abstract

The TNF family cytokine TL1A (Tnfsf15) costimulates T cells and type 2 innate lymphocytes (ILC2) through its receptor DR3 (Tnfrsf25). DR3-deficient mice have reduced T cell accumulation at the site of inflammation and reduced ILC2-dependent immune responses in a number of models of autoimmune and allergic diseases. In allergic lung disease models, immunopathology and local Th2 and ILC2 accumulation is reduced in DR3-deficient mice despite normal systemic priming of Th2 responses and generation of T cells secreting IL-13 and IL-4, prompting the question of whether TL1A promotes the development of other T cell subsets that secrete cytokines to drive allergic disease. In this study, we find that TL1A potently promotes generation of murine T cells producing IL-9 (Th9) by signaling through DR3 in a cell-intrinsic manner. TL1A enhances Th9 differentiation through an IL-2 and STAT5-dependent mechanism, unlike the TNF-family member OX40, which promotes Th9 through IL-4 and STAT6. Th9 differentiated in the presence of TL1A are more pathogenic, and endogenous TL1A signaling through DR3 on T cells is required for maximal pathology and IL-9 production in allergic lung inflammation. Taken together, these data identify TL1A-DR3 interactions as a novel pathway that promotes Th9 differentiation and pathogenicity. TL1A may be a potential therapeutic target in diseases dependent on IL-9.

Indexed as

AnimalsAsthmaCell DifferentiationInflammationInterleukin-13Interleukin-4Interleukin-9MiceMice, KnockoutReceptors, Tumor Necrosis Factor, Member 25Signal TransductionT-Lymphocytes, Helper-InducerTumor Necrosis Factor Ligand Superfamily Member 15Interleukin-13Interleukin-4Interleukin-9Receptors, Tumor Necrosis Factor, Member 25Tnfrsf25 protein, mouseTnfsf15 protein, mouseTumor Necrosis Factor Ligand Superfamily Member 15

Identifiers

PMID25786692
PMCPMC5112176
OpenAlexW2129438140

What OpenQuestion holds

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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.