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