Evidence map›Paper›PMID 25989458›Full record

ArticleEuropean journal of immunology2015

Allele-sensitive mutant, Itkas, reveals that Itk kinase activity is required for Th1, Th2, Th17, and iNKT-cell cytokine production.

Arun Kannan, YongChan Lee, Qian Qi, Weishan Huang, Ah-Reum Jeong, Sarah Ohnigian, Avery August

Open access · bronzeAbstract read
In one paragraph

Article in European journal of immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.4field-weighted citation impact, top 37% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. The kinase ITK controls a CaScience signaling · 2024
    Article
  4. Article
  5. Article
  6. TCR/ITK Signaling in Type 1 Regulatory T cells.Advances in experimental medicine and biology · 2021
    Article
  7. Tuning T helper cell differentiation by ITK.Biochemical Society transactions · 2020
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
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

7 authors at 2 institutions in 1 country.

Arun KannanCenter for Infection and Pathobiology, Department of Microbiology and Immunology, Cornell University, Ithaca, NY, USA.
YongChan LeeCenter for Infection and Pathobiology, Department of Microbiology and Immunology, Cornell University, Ithaca, NY, USA.
Qian QiCenter for Infection and Pathobiology, Department of Microbiology and Immunology, Cornell University, Ithaca, NY, USA.
Weishan HuangCenter for Infection and Pathobiology, Department of Microbiology and Immunology, Cornell University, Ithaca, NY, USA.
Ah-Reum JeongKeck School of Medicine of University of Southern California, Los Angeles, CA, USA.
Sarah OhnigianCenter for Infection and Pathobiology, Department of Microbiology and Immunology, Cornell University, Ithaca, NY, USA.
Avery AugustCenter for Infection and Pathobiology, Department of Microbiology and Immunology, Cornell University, Ithaca, NY, USA.
Cornell University · USUniversity of Southern California · 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
Selective Aryl Hydrocarbon Receptor Modulators and T cell Effector FunctionR21AI108958 · NIAID · CORNELL UNIVERSITY · PI AUGUST, AVERY · 2014 to 2015
$430k
ITK Mast Cells and Allergic Airway ResponsesR56AI065566 · NIAID · PENNSYLVANIA STATE UNIVERSITY, THE · PI AUGUST, AVERY · 2006 to 2006
$345k
NIAID NIH HHS AI065566NIAID NIH HHS AI51626NIAID NIH HHS R01 AI051626NIAID NIH HHS R01 AI065566NIAID NIH HHS R01 AI073955NIAID NIH HHS R21 AI108958NIAID NIH HHS R56 AI065566
6 · The paper itself

Abstract

Itk(-/-) mice exhibit defects in the activation, development, and function of CD4(+) and CD8(+) T cells and iNKT cells. These and other defects in these mice make it difficult to uncouple the developmental versus functional requirement of Itk signaling. Here, we report an allele-sensitive mutant of Itk (Itkas) whose catalytic activity can be selectively inhibited by analogs of the PP1 kinase inhibitor. We show that Itkas behaves like WT Itk in the absence of the inhibitor and can rescue the development of Itk(-/-) T cells in mice. Using mice carrying Itkas, we show using its inhibitor that Itk activity is required not only for Th2, Th17, and iNKT-cell cytokine production, but also surprisingly, for Th1 cytokine production. This work has important implications for understanding the role of Itk signaling in the development versus function of iNKT cells, Th1, Th2, and Th17 cells.

Indexed as

AllelesMutationAnimalsCytokinesMiceMice, KnockoutNatural Killer T-CellsProtein-Tyrosine KinasesSignal TransductionTh17 CellsTh1 CellsTh2 CellsCytokinesemt protein-tyrosine kinaseProtein-Tyrosine KinasesAllele-sensitiveCytokinesiNKT-cellItkKinase inhibitorTec kinase

Identifiers

PMID25989458
PMCPMC5730406
OpenAlexW2157658648

What Socratic 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 Socratic graph.