ArticleBMC genomics2009
Transcriptional signatures of Itk-deficient CD3+, CD4+ and CD8+ T-cells.
Article in BMC genomics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
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- Article
- Interleukin-2-Inducible T-Cell Kinase Deficiency-New Patients, New Insight?Frontiers in immunology · 2018Review
- B Cell Receptor Activation Predominantly Regulates AKT-mTORC1/2 Substrates Functionally Related to RNA Processing.PloS one · 2016Article
- [MUW researcher of the month].Wiener klinische Wochenschrift · 2015Article
- Interleukin-2-inducible T-cell kinase (ITK) deficiency - clinical and molecular aspects.Journal of clinical immunology · 2014Review
- Counter-regulation of T cell effector function by differentially activated p38.The Journal of experimental medicine · 2014Article
- Bach2 maintains T cells in a naive state by suppressing effector memory-related genes.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Partial defects of T-cell development associated with poor T-cell function.The Journal of allergy and clinical immunology · 2013Review
- DEF6, a novel substrate for the Tec kinase ITK, contains a glutamine-rich aggregation-prone region and forms cytoplasmic granules that co-localize with P-bodies.The Journal of biological chemistry · 2012Article
- Loss-of-function mutations within the IL-2 inducible kinase ITK in patients with EBV-associated lymphoproliferative diseases.Leukemia · 2012Article
- Functional characterization of protein domains common to animal viruses and mouse.BMC genomics · 2011Article
- T-cell signaling regulated by the Tec family kinase, Itk.Cold Spring Harbor perspectives in biology · 2010Review
- Multiplex meta-analysis of RNA expression to identify genes with variants associated with immune dysfunction.Journal of the American Medical Informatics Association : JAMIAArticle
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
backgroundThe Tec-family kinase Itk plays an important role during T-cell activation and function, and controls also conventional versus innate-like T-cell development. We have characterized the transcriptome of Itk-deficient CD3+ T-cells, including CD4+ and CD8+ subsets, using Affymetrix microarrays.
resultsThe largest difference between Itk-/- and Wt CD3+ T-cells was found in unstimulated cells, e.g. for killer cell lectin-like receptors. Compared to anti-CD3-stimulation, anti-CD3/CD28 significantly decreased the number of transcripts suggesting that the CD28 co-stimulatory pathway is mainly independent of Itk. The signatures of CD4+ and CD8+ T-cell subsets identified a greater differential expression than in total CD3+ cells. Cyclosporin A (CsA)-treatment had a stronger effect on transcriptional regulation than Itk-deficiency, suggesting that only a fraction of TCR-mediated calcineurin/NFAT-activation is dependent on Itk. Bioinformatic analysis of NFAT-sites of the group of transcripts similarly regulated by Itk-deficiency and CsA-treatment, followed by chromatin-immunoprecipitation, revealed NFATc1-binding to the Bub1, IL7R, Ctla2a, Ctla2b, and Schlafen1 genes. Finally, to identify transcripts that are regulated by Tec-family kinases in general, we compared the expression profile of Itk-deficient T-cells with that of Btk-deficient B-cells and a common set of transcripts was found.
conclusionTaken together, our study provides a general overview about the global transcriptional changes in the absence of Itk.
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Registered trials
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.