Evidence map›Paper›PMID 23768572›Full record

ArticleThe Journal of allergy and clinical immunology2013

IL-2-inducible T-cell kinase modulates TH2-mediated allergic airway inflammation by suppressing IFN-γ in naive CD4+ T cells.

Arun K Kannan, Nisebita Sahu, Sunish Mohanan, Sonia Mohinta, Avery August

Open access · greenAbstract read
In one paragraph

Article in The Journal of allergy and clinical immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

25 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. The kinase ITK controls a CaScience signaling · 2024
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  10. Review
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  18. Lack of allergy to timothy grass pollen is not a passive phenomenon but associated with the allergen-specific modulation of immune reactivity.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2016
    Article
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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

5 authors at 2 institutions in 1 country.

Arun K KannanDepartment of Microbiology and Immunology, Cornell University, Ithaca, NY.
Nisebita Sahu
Sunish Mohanan
Sonia Mohinta
Avery August
Cornell University · USPennsylvania State University · US

Funding

Tyrosine Kinase ITK in Experimental Allergic AsthmaR01AI051626 · NIAID · PENNSYLVANIA STATE UNIVERSITY-UNIV PARK · PI AUGUST, AVERY · 2003 to 2012
$3.6M
Eosinophils and Allergic Airway ResponsesR01AI073955 · NIAID · PENNSYLVANIA STATE UNIVERSITY, THE · PI AUGUST, AVERY · 2008 to 2012
$1.9M
ITK Mast Cells and Allergic Airway ResponsesR01AI065566 · NIAID · PENNSYLVANIA STATE UNIVERSITY, THE · PI AUGUST, AVERY · 2007 to 2011
$1.5M
ITK Mast Cells and Allergic Airway ResponsesR56AI065566 · NIAID · PENNSYLVANIA STATE UNIVERSITY, THE · PI AUGUST, AVERY · 2006 to 2006
$345k
NIAID NIH HHS AI051626NIAID NIH HHS AI065566NIAID NIH HHS R01 AI051626NIAID NIH HHS R01 AI065566NIAID NIH HHS R01 AI073955NIAID NIH HHS R56 AI065566
6 · The paper itself

Abstract

backgroundAsthma is a predominantly TH2 cell-dominated inflammatory disease characterized by airway inflammation and a major public health concern affecting millions of persons. The Tec family tyrosine kinase IL-2-inducible T-cell kinase (Itk) is primarily expressed in T cells and critical for the function and differentiation of TH cells. Itk(-/-) mice have a defective TH2 response and are not susceptible to allergic asthma.

objectiveWe sought to better understand the role of Itk signaling in TH differentiation programs and in the development and molecular pathology of allergic asthma.

methodsUsing a murine model of allergic airway inflammation, we dissected the role of Itk in regulating TH cell differentiation through genetic ablation of critical genes, chromatin immunoprecipitation assays, and house dust mite-driven allergic airway inflammation.

resultsPeripheral naive Itk(-/-) CD4(+) T cells have substantially increased transcripts and expression of the prototypic TH1 genes Eomesodermin, IFN-γ, T-box transcription factor (T-bet), and IL-12Rβ1. Removal of IFN-γ on the Itk(-/-) background rescues expression of TH2-related genes in TH cells and allergic airway inflammation in Itk(-/-) mice. Furthermore, small hairpin RNA-mediated knockdown of Itk in human peripheral blood T cells results in increased expression of mRNA for IFN-γ and T-bet and reduction in expression of IL-4.

conclusionOur results indicate that Itk signals suppress the expression of IFN-γ in naive CD4(+) T cells, which in a positive feed-forward loop regulates the expression of TH1 factors, such as T-bet and Eomesodermin, and suppress development of TH2 cells and allergic airway inflammation.

Indexed as

AnimalsAsthmaCD4-Positive T-LymphocytesCell DifferentiationChromatin ImmunoprecipitationFemaleHumansHypersensitivityInflammationInterferon-gammaMaleMiceProtein-Tyrosine KinasesPyroglyphidaeTh1 CellsTh2 Cellsemt protein-tyrosine kinaseInterferon-gammaProtein-Tyrosine KinasesAHRAirways hyperresponsivenessallergic asthmaAntigen-presenting cellAPCBALFBronchoalveolar lavage fluidChIPChromatin immunoprecipitationCNSConserved noncoding sequenceDKODouble knockoutEomesEomesoderminHDMHouse dust miteIFN-γIL-2–inducible T-cell kinaseItkPhorbol 12-myristate 13-acetate/ionomycinP/IqPCRQuantitative PCRshRNASmall hairpin RNAT-betT-box transcription factorT-cell receptorTCRTec kinaseT(H)2Wild typeWT

Identifiers

PMID23768572
PMCPMC4033298
OpenAlexW2004697163

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.