The initiation of biochemical signal transduction following ligation of surface receptors with intrinsic cytoplasmic tyrosine kinase activity is common for many cell types. T lymphocytes also require activation of tyrosine kinases following T cell receptor (TCR) ligation for maximal stimulation. However, the TCR has no intrinsic tyrosine kinase activity. Instead, the TCR must rely on cytoplasmic tyrosine kinases that localize to the TCR complex and initiate TCR-mediated signaling events. Although much has been learned regarding how these cytosolic tyrosine kinases are activated and recruited to the TCR complex, relatively little is understood about how these initial events are translated into transcriptional activation of genes that regulate cytokine production, cell proliferation, and cell death. Recently, it has become clear that the class of intracellular molecules known collectively as adapter proteins, molecules with modular domains capable of recruiting additional proteins but that exhibit no intrinsic enzymatic activity, serve to couple proximal biochemical events initiated by TCR ligation with more distal signaling pathways.

中文翻译：

---

通过衔接蛋白整合T细胞受体依赖性信号通路。

表面受体与固有的胞质酪氨酸激酶活性连接后，生化信号转导的启动对于许多细胞类型而言是常见的。为了最大程度地刺激，在T细胞受体（TCR）连接后，T淋巴细胞还需要激活酪氨酸激酶。但是，TCR没有固有的酪氨酸激酶活性。相反，TCR必须依赖定位于TCR复合体并启动TCR介导的信号转导事件的胞质酪氨酸激酶。尽管关于这些胞质酪氨酸激酶是如何被激活和募集到TCR复合体的知识很多，但是对于这些初始事件如何转化为调节细胞因子产生，细胞增殖和细胞死亡的基因的转录激活的了解相对较少。最近，