Evidence map›Paper›PMID 26936133›Full record

ArticleNature communications2016

Itk is required for Th9 differentiation via TCR-mediated induction of IL-2 and IRF4.

Julio Gomez-Rodriguez, Françoise Meylan, Robin Handon, Erika T Hayes, Stacie M Anderson, Martha R Kirby, Richard M Siegel, Pamela L Schwartzberg

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
5.9field-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

51 citing papers in PubMed, 81 citations in OpenAlex.

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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

8 authors at 3 institutions in 1 country.

Julio Gomez-RodriguezNational Human Genome Research Institute, National Institutes of Health, 49 Convent Drive, Bethesda, Maryland 20892, USA.
Françoise MeylanNational Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, 9000 Rockville Pike, Bethesda, Maryland 20892, USA.
Robin HandonNational Human Genome Research Institute, National Institutes of Health, 49 Convent Drive, Bethesda, Maryland 20892, USA.
Erika T HayesNational Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, 9000 Rockville Pike, Bethesda, Maryland 20892, USA.
Stacie M AndersonNational Human Genome Research Institute, National Institutes of Health, 49 Convent Drive, Bethesda, Maryland 20892, USA.
Martha R KirbyNational Human Genome Research Institute, National Institutes of Health, 49 Convent Drive, Bethesda, Maryland 20892, USA.
Richard M SiegelNational Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, 9000 Rockville Pike, Bethesda, Maryland 20892, USA.
Pamela L SchwartzbergNational Human Genome Research Institute, National Institutes of Health, 49 Convent Drive, Bethesda, Maryland 20892, USA.
National Institutes of Health · USNational Human Genome Research Institute · USNational Institute of Arthritis and Musculoskeletal and Skin Diseases · US

Funding

Clinical Support Services for the NIAMS Intramural Research ProgramZIDAR041180 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI COLBERT, ROBERT · 2009 to 2025
$119.2M
Genetic and Biochemical Approaches to Tyrosine Kinase FunctionZIAHG000123 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI SCHWARTZBERG, PAMELA · 2009 to 2018
$20.8M
NHGRI/DIR Flow Cytometry CoreZICHG200350 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI ANDERSON, STACIE · 2010 to 2025
$16.3M
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
Intramural NIH HHS
6 · The paper itself

Abstract

Th9 cells produce interleukin (IL)-9, a cytokine implicated in allergic asthma and autoimmunity. Here we show that Itk, a mediator of T cell receptor signalling required for Th2 immune responses and the development of asthma, is a positive regulator of Th9 differentiation. In a model of allergic lung disease, Itk-deficient mice show reduced pulmonary inflammation and IL-9 production by T cells and innate lymphoid type 2 cells (ILC2), despite normal early induction of ILC2s. In vitro, Itk(-/-) CD4(+) T cells do not produce IL-9 and have reduced levels of IRF4 (Interferon Regulator Factor 4), a critical transcription factor for effector T cell function. Both IL-9 and IRF4 expression are rescued by either IL-2 or constitutively active STAT5, but not NFATc1. STAT5 binds the Irf4 promoter, demonstrating one mechanism by which IL-2 rescues weakly activated T cells. Itk inhibition also reduces IL-9 expression by human T cells, implicating ITK as a key regulator of Th9 induction.

Indexed as

AnimalsCD4-Positive T-LymphocytesCell DifferentiationFemaleGene Expression RegulationInterferon Regulatory Factor-4Interferon Regulatory FactorsInterleukin-2Lung DiseasesMaleMiceMice, KnockoutPapainProtein KinasesProtein-Tyrosine Kinasesemt protein-tyrosine kinaseInterferon Regulatory Factor-4Interferon Regulatory FactorsInterleukin-2PapainProtein KinasesProtein-Tyrosine KinasesSmok1 protein, mouse

Identifiers

PMID26936133
PMCPMC4782063
OpenAlexW2332925781

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.