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PKC- is a Drug Target for Prevention of T Cell-Mediated Autoimmunity and Allograft Rejection

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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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Keywords: APC; Activationinduced cell death; DAG; EAE; MHC; MOG; PKC-; T cell receptor; T cells; TCR; TCR signaling; airway hyperresponsiveness; antigen presenting cells; autoimmunity; central SMAC; collagen-induced arthritis; diacylglycerol; distal SMAC; experimental autoimmune encephalitis; histocompatibility complex; myelin oligodendrocyte glycoprotein; peripheral SMAC; protein tyrosine kinase; transplantation rejection

Document Type: Research Article

Publication date: December 1, 2010

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  • This journal is devoted to timely reviews of experimental and clinical studies in the field of endocrine, metabolic, and immune disorders. Specific emphasis is placed on humoral and cellular targets for natural, synthetic, and genetically engineered drugs that enhance or impair endocrine, metabolic, and immune parameters and functions. Topics related to the neuroendocrine-immune axis are given special emphasis in view of the growing interest in stress-related, inflammatory, autoimmune, and degenerative disorders.
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