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Immunol Lett. 2009 Sep 22;126(1-2):54-9. doi: 10.1016/j.imlet.2009.07.014. Epub 2009 Aug 12.

PKCtheta and Itk functionally interact during primary mouse CD3+ T cell activation.

Author information

1
Department for Medical Genetics, Molecular and Clinical Pharmacology, Medical University of Innsbruck, Innsbruck, Austria. Nikolaus.Thuille@i-med.ac.at

Abstract

PKCtheta serine/threonine and Itk tyrosine protein kinases have been implicated in T lymphocyte signal transmission. We observed a PKCtheta/Itk complex after T cell activation, raising the possibility that PKCtheta and Itk might interact functionally during T cell development and response. To address this question PKCtheta/Itk double knockout mice were generated and T cell activation responses were compared to single deficiencies as well as to wild type controls. Consistent with previous reports, Itk and PKCtheta are required in modulating CD3(+) T cell cytokine secretion responses ex vivo. Itk- and PKCtheta-deficient cells show impaired NFAT/AP-1 and NF-kappaB transactivation responses, however the combined loss, did not exceed but partially rescue the strong NFAT and NF-kappaB activation defects observed in Itk(-/-) single-deficient T cells. Taken together, this provides evidence for a more complex functional crosstalk between Itk and PKCtheta during T cell receptor signalling then previously anticipated.

PMID:
19682494
DOI:
10.1016/j.imlet.2009.07.014
[Indexed for MEDLINE]

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