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Molecular and Cellular Biology, April 2000, p. 2933-2940, Vol. 20, No. 8
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Protein Kinase C-theta Participates in NF-kappa B Activation Induced by CD3-CD28 Costimulation through Selective Activation of Ikappa B Kinase beta

Xin Lin, Alison O'Mahony, Yajun Mu, Romas Geleziunas, and Warner C. Greene*

Gladstone Institute of Virology and Immunology, Departments of Medicine and Microbiology and Immunology, University of California, San Francisco, California 94141

Received 8 September 1999/Returned for modification 18 October 1999/Accepted 10 January 2000

The NF-kappa B/Rel family of eukaryotic transcription factors plays an essential role in the regulation of inflammatory, antiapoptotic, and immune responses. NF-kappa B is activated by many stimuli including costimulation of T cells with ligands specific for the T-cell receptor (TCR)-CD3 complex and CD28 receptors. However, the signaling intermediates that transduce these costimulatory signals from the TCR-CD3 and CD28 surface receptors leading to nuclear NF-kappa B expression are not well defined. We now show that protein kinase C-theta (PKC-theta ), a novel PKC isoform, plays a central role in a signaling pathway induced by CD3-CD28 costimulation leading to activation of NF-kappa B in Jurkat T cells. We find that expression of a constitutively active mutant of PKC-theta potently induces NF-kappa B activation and stimulates the RE/AP composite enhancer from the interleukin-2 gene. Conversely, expression of a kinase-deficient mutant or antisense PKC-theta selectively inhibits CD3-CD28 costimulation, but not tumor necrosis factor alpha-induced activation of NF-kappa B in Jurkat T cells. The induction of NF-kappa B by PKC-theta is mediated through the activation of Ikappa B kinase beta  (IKKbeta ) in the absence of detectable IKKalpha stimulation. PKC-theta acts directly or indirectly to stimulate phosphorylation of IKKbeta , leading to activation of this enzyme. Together, these results implicate PKC-theta in one pathway of CD3-CD28 costimulation leading to NF-kappa B activation that is apparently distinct from that involving Cot and NF-kappa B-inducing kinase (NIK). PKC-theta activation of NF-kappa B is mediated through the selective induction of IKKbeta , while the Cot- and NIK-dependent pathway involves induction of both IKKalpha and IKKbeta .

* Corresponding author. Mailing address: Gladstone Institute of Virology and Immunology, P.O. Box 419100, San Francisco, CA 94141-9100. Phone: (415) 695-3800. Fax: (415) 826-1817. E-mail: wgreene{at}gladstone.ucsf.edu.

Molecular and Cellular Biology, April 2000, p. 2933-2940, Vol. 20, No. 8
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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