The Journal of Experimental Medicine
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A correction to this article has been published: J. Exp. Med. 198 (1) 183
Published 2 June 2003. doi:10.1084/jem.20020234
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© Rockefeller University Press, 0022-1007/2003/6/1525 $5.00
The Journal of Experimental Medicine, Volume 197, Number 11, 1525-1535

Protein Kinase C {theta} Affects Ca2+ Mobilization and NFAT Activation in Primary Mouse T Cells

Christa Pfeifhofer1, Kurt Kofler1, Thomas Gruber1, Nassim Ghaffari Tabrizi1, Christina Lutz1, Karl Maly2, Michael Leitges3 and Gottfried Baier1

1 Institute of Medical Biology and Human Genetics, University of Innsbruck, A-6020 Innsbruck, Austria
2 Institute of Medical Biochemistry, University of Innsbruck, A-6020 Innsbruck, Austria
3 Max-Planck Institute for Experimental Endocrinology, D-30625 Hannover, Germany

Address correspondence to Gottfried Baier, Institute of Medical Biology and Human Genetics, University of Innsbruck, Schoepfstraße 41, A-6020 Innsbruck, Austria. Phone: 43-512-507-3451; Fax: 43-512-507-2861; E-mail: Gottfried.Baier{at}uibk.ac.at

Protein kinase C (PKC){theta} is an established component of the immunological synapse and has been implicated in the control of AP-1 and NF-{kappa}B. To study the physiological function of PKC{theta}, we used gene targeting to generate a PKC{theta} null allele in mice. Consistently, interleukin 2 production and T cell proliferative responses were strongly reduced in PKC{theta}-deficient T cells. Surprisingly, however, we demonstrate that after CD3/CD28 engagement, deficiency of PKC{theta} primarily abrogates NFAT transactivation. In contrast, NF-{kappa}B activation was only partially reduced. This NFAT transactivation defect appears to be secondary to reduced inositol 1,4,5-trisphosphate generation and intracellular Ca2+ mobilization. Our finding suggests that PKC{theta} plays a critical and nonredundant role in T cell receptor–induced NFAT activation.

Key Words: T lymphocyte • PKC{theta} • TCR/CD3 • Ca2+ response • NFAT


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