Kwon Myung-Ja, Wang Ruiqing, Ma Jian, Sun Zuoming
Beckman Research Institute of the City of Hope, Duarte, CA 91010, Los Angeles, USA.
Endocr Metab Immune Disord Drug Targets. 2010 Dec;10(4):367-72. doi: 10.2174/1871530311006040367.
Protein kinase C theta (PKC-θ) is a key kinase in mediating T cell receptor (TCR) signals. PKC-θ activated by T cell receptor (TCR) engagement translocates to immunological synapses and regulates the activation of transcriptional factors NFκB, AP-1, and NFAT. These transcription factors then activate target genes such as IL-2. T cells deficient in PKC-θ display defects in T cell activation, survival, activation-induced cell death, and the differentiation into inflammatory T cells, such as Th2 and Th17 cells both in vitro and in vivo. Since these effector T helper cells are responsible for mediating autoimmunity, selective inhibition of PKC-θ is considered a treatment for prevention of autoimmune diseases and allograft rejection.
蛋白激酶Cθ（PKC-θ）是介导T细胞受体（TCR）信号的关键激酶。T细胞受体（TCR）结合激活的PKC-θ转位至免疫突触，调节转录因子NFκB、AP-1和NFAT的激活。这些转录因子随后激活诸如白细胞介素-2等靶基因。PKC-θ缺陷的T细胞在体外和体内的T细胞激活、存活、激活诱导的细胞死亡以及向炎性T细胞（如Th2和Th17细胞）的分化方面均表现出缺陷。由于这些效应性辅助性T细胞负责介导自身免疫，因此选择性抑制PKC-θ被认为是预防自身免疫性疾病和同种异体移植排斥的一种治疗方法。
