Gomez-Rodriguez Julio, Readinger Julie A, Viorritto Irene C, Mueller Kristen L, Houghtling Richard A, Schwartzberg Pamela L
National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Immunol Rev. 2007 Aug;218:45-64. doi: 10.1111/j.1600-065X.2007.00534.x.
The Tec family non-receptor tyrosine kinases have been recognized for their roles in the regulation of phospholipase C-gamma and Ca(2+) mobilization downstream from antigen receptors on lymphocytes. Recent data, however, show that the Tec family kinase interleukin-2-inducible T-cell kinase (Itk) also participates in pathways regulating the actin cytoskeleton and 'inside-out' signaling to integrins downstream from the T-cell antigen receptor. Data suggest that Itk may function in a kinase-independent fashion to regulate proper recruitment of the Vav1 guanine nucleotide exchange factor. By enhancing actin cytoskeleton reorganization, recruitment of signaling molecules to the immune synapse, and integrin clustering in response to both antigen and chemokine receptors, the Tec kinases serve as modulators or amplifiers that can increase the duration of T-cell signaling and regulate T-cell functional responses.
Tec家族非受体酪氨酸激酶在调节淋巴细胞抗原受体下游的磷脂酶C-γ和Ca(2+)动员方面的作用已得到认可。然而，最近的数据表明，Tec家族激酶白细胞介素-2诱导型T细胞激酶（Itk）也参与调节肌动蛋白细胞骨架的途径以及T细胞抗原受体下游整合素的“由内向外”信号传导。数据表明，Itk可能以不依赖激酶的方式发挥作用，以调节Vav1鸟嘌呤核苷酸交换因子的正确募集。通过增强肌动蛋白细胞骨架重组、信号分子向免疫突触的募集以及对抗原和趋化因子受体的反应中整合素的聚集，Tec激酶充当调节剂或放大器，可以增加T细胞信号传导的持续时间并调节T细胞功能反应。
