Abstract
Protein kinase C theta (PKC-) is a key kinase in mediating T cell receptor (TCR) signals. PKC- activated by T cell receptor (TCR) engagement translocates to immunological synapses and regulates the activation of transcriptional factors NF-κB, AP-1, and NFAT. These transcription factors then activate target genes such as IL-2. T cells deficient in PKC- display defects in T cell activation, survival, activation-induced cell death, and the differentiation into inflammatory T cells, both in vitro and in vivo. Since these effector T helper cells are responsible for mediating autoimmunity, selective inhibition of PKC- is considered a treatment for prevention of autoimmune diseases and allograft rejection.
Keywords: PKC-, T cells, TCR signaling, autoimmunity, transplantation rejection, T cell receptor, TCR, antigen presenting cells, APC, histocompatibility complex, MHC, protein tyrosine kinase, diacylglycerol, DAG, central SMAC, peripheral SMAC, distal SMAC, Activationinduced cell death, airway hyperresponsiveness, myelin oligodendrocyte glycoprotein, MOG, experimental autoimmune encephalitis, EAE, collagen-induced arthritis
Endocrine, Metabolic & Immune Disorders - Drug Targets
Title: PKC-θ is a Drug Target for Prevention of T Cell-Mediated Autoimmunity and Allograft Rejection
Volume: 10 Issue: 4
Author(s): Myung-Ja Kwon, Ruiqing Wang, Jian Ma and Zuoming Sun
Affiliation:
Keywords: PKC-, T cells, TCR signaling, autoimmunity, transplantation rejection, T cell receptor, TCR, antigen presenting cells, APC, histocompatibility complex, MHC, protein tyrosine kinase, diacylglycerol, DAG, central SMAC, peripheral SMAC, distal SMAC, Activationinduced cell death, airway hyperresponsiveness, myelin oligodendrocyte glycoprotein, MOG, experimental autoimmune encephalitis, EAE, collagen-induced arthritis
Abstract: Protein kinase C theta (PKC-) is a key kinase in mediating T cell receptor (TCR) signals. PKC- activated by T cell receptor (TCR) engagement translocates to immunological synapses and regulates the activation of transcriptional factors NF-κB, AP-1, and NFAT. These transcription factors then activate target genes such as IL-2. T cells deficient in PKC- display defects in T cell activation, survival, activation-induced cell death, and the differentiation into inflammatory T cells, both in vitro and in vivo. Since these effector T helper cells are responsible for mediating autoimmunity, selective inhibition of PKC- is considered a treatment for prevention of autoimmune diseases and allograft rejection.
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Cite this article as:
Kwon Myung-Ja, Wang Ruiqing, Ma Jian and Sun Zuoming, PKC-θ is a Drug Target for Prevention of T Cell-Mediated Autoimmunity and Allograft Rejection, Endocrine, Metabolic & Immune Disorders - Drug Targets 2010; 10 (4) . https://dx.doi.org/10.2174/1871530311006040367
DOI https://dx.doi.org/10.2174/1871530311006040367 |
Print ISSN 1871-5303 |
Publisher Name Bentham Science Publisher |
Online ISSN 2212-3873 |
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