alexa PKCθ is a Key Regulator of T-cell Behavior and a
ISSN: 2155-9899

Journal of Clinical & Cellular Immunology
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Review Article

PKCθ is a Key Regulator of T-cell Behavior and a Drug Target for T cell-mediated Diseases

Noah Isakov*
The Shraga Segal Department of Microbiology, Immunology and Genetics, Faculty of Health Sciences and the Cancer Research Center, Ben Gurion University of the Negev, Beer Sheva, Israel
Corresponding Author : Dr. Noah Isakov
The Shraga Segal Department of Microbiology
Immunology and Genetics, Faculty of Health Sciences
Ben Gurion University of the Negev
P.O.B. 653, Beer Sheva 84105, Israel
Tel: 97286477267
Fax: 97286477626
E-mail: [email protected]
Received: September 20, 2012; Accepted: October 30, 2012; Published: November 06, 2012
Citation: Isakov N (2012) PKCθ is a Key Regulator of T-cell Behavior and a Drug Target for T cell-mediated Diseases. J Clin Cell Immunol S12:008. doi:10.4172/2155-9899.S12-008
Copyright: © 2012 Isakov N. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

The protein kinase C-theta (PKCθ) isoform is a member of the calcium-independent novel PKC subfamily of serine/threonine kinases. It is an essential regulatory enzyme in mature T lymphocytes, where it plays a key role in coupling the activated TCR and the CD28 costimulatory receptor to their downstream signaling pathways. TCR/ CD28 engagement induces the translocation of PKCθ to the center of the immunological synapse where it undergoes posttranslational modifications and becomes fully active. The activated PKCθ then initiates signaling pathways leading to the activation of transcription factors, including NF-κB, AP-1 and NF-AT that are essential for the survival, activation and differentiation of T cells. While PKCθ ablation was found to impair a wide range of in vitro responses of T cells, in vivo studies in Prkcq-/- mice revealed that distinct T cell subpopulations differ in their requirements for PKCθ and that PKCθ has a selective role in different immune responses. Thus, PKCθ participates in cellular mechanisms leading to excessive inflammatory responses, autoimmunity, and graft vs host (GvH) disease, but is dispensable for beneficial immune responses against viruses and during graft vs leukemia responses. These studies suggest that PKCθ may serve as a potential drug target for catalytic and allosteric inhibitors in selected T cell-mediated diseases, and that fine-tuning of PKCθ-dependent functions may help prevent autoimmunity and GvH, without impairing the ability of T cells to eradicate viral-infected and transformed cells.

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