Foster G R
Liver Unit, Imperial College School of Medicine at St. Mary's, London, England.
Semin Liver Dis. 1997;17(4):287-95. doi: 10.1055/s-2007-1007205.
The Type I interferons are a group of related glycoproteins that play a key role in host defenses against viral infections. The interferons bind to a cell surface receptor and initiate the transcription of a wide range of proteins that have potent antiviral properties. The mechanism by which interferon binding to the cell surface initiates gene transcription has recently been elucidated and involves activation of protein kinases (JAK 1 and Tyk 2) followed by phosphorylation and activation of transcriptional regulators (the STAT proteins). These signal transduction molecules are not unique to the interferon signaling pathway, and other cytokines as diverse as erythropoietin and IL-2 use the same, or related proteins. To overcome the antiviral effects of the type I interferons, some viruses that cause chronic infections have developed interferon inhibitors that reduce the effectiveness of endogenous and exogenous interferon.
I型干扰素是一组相关的糖蛋白，在宿主抵御病毒感染的防御机制中发挥关键作用。干扰素与细胞表面受体结合，并启动多种具有强大抗病毒特性的蛋白质的转录。干扰素与细胞表面结合启动基因转录的机制最近已被阐明，涉及蛋白激酶（JAK 1和Tyk 2）的激活，随后转录调节因子（STAT蛋白）发生磷酸化并被激活。这些信号转导分子并非I型干扰素信号通路所特有，其他多种细胞因子，如促红细胞生成素和白细胞介素-2，也使用相同或相关的蛋白质。为了克服I型干扰素的抗病毒作用，一些导致慢性感染的病毒已开发出干扰素抑制剂，以降低内源性和外源性干扰素的有效性。
