Evidence map›Paper›PMID 22403441›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

A unique role for ITK in survival of invariant NKT cells associated with the p53-dependent pathway in mice.

Qian Qi, Weishan Huang, Yuting Bai, Gabriel Balmus, Robert S Weiss, Avery August

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Itk signals promote neuroinflammation by regulating CD4+ T-cell activation and trafficking.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  14. Review
  15. Article
  16. Article
  17. Partial defects of T-cell development associated with poor T-cell function.The Journal of allergy and clinical immunology · 2013
    Review
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

6 authors at 2 institutions in 1 country.

Qian QiCenter for Molecular Immunology and Infectious Disease, The Pennsylvania State University, University Park, PA 16801, USA.
Weishan Huang
Yuting Bai
Gabriel Balmus
Robert S Weiss
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

Invariant NKT (iNKT) cells play important roles in the immune response. ITK and TXK/RLK are Tec family kinases that are expressed in iNKT cells; the expression level of ITK is ∼7-fold higher than that of TXK. Itk(-/-) mice have reduced iNKT cell frequency and numbers, with defects in development and cytokine secretion that are exacerbated in Itk/Txk double-knockout mice. In contrast, there is no iNKT cell defect in Txk(-/-) mice. To determine whether ITK and TXK play distinct roles in iNKT cell development and function, we examined mice that overexpress TXK in T cells at levels similar to Itk. Overexpression of TXK rescues the maturation and cytokine secretion of Itk(-/-) iNKT cells, as well as altered expression of transcription factors T-bet, eomesodermin, and PLZF. In contrast, the increased apoptosis observed in Itk(-/-) splenic iNKT cells is not affected by TXK overexpression, likely due to the lack of effect on the elevated expression of p53 regulated proapoptotic pathways Fas, Bax, and Bad in those cells. Supporting this idea, p53(-/-) and Bax(-/-) mice have increased splenic iNKT cells. Our results suggest that TXK plays an overlapping role with ITK in iNKT cell development and function but that ITK also has a unique function in the survival of iNKT cells, likely via a p53-dependent pathway.

Indexed as

AnimalsApoptosisCell SurvivalCytokinesGalactosylceramidesGene Expression RegulationMiceMice, KnockoutNatural Killer T-CellsPrimary Cell CultureProtein-Tyrosine KinasesSignal TransductionSpleenTranscription FactorsTumor Suppressor Protein p53alpha-galactosylceramideCytokinesemt protein-tyrosine kinaseGalactosylceramidesProtein-Tyrosine KinasesTec protein-tyrosine kinaseTranscription FactorsTumor Suppressor Protein p53

Identifiers

PMID22403441
PMCPMC3337705
OpenAlexW2111661519

What OpenQuestion holds

Textmetadata
LicenceTDM
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.