摘要
信号抑制因子(SOCS)是在细胞因子诱导下依赖JAK/STAT通路的信号传导而产生的,继而抑制细胞因子的信号传导,因此SOCS蛋白质被认为可以形成局部经典负反馈回路。IFN是由辅助性T细胞I类亚群和自然杀伤细胞等分泌的一种细胞因子,具有多种免疫调节功能。在炎症反应中IFN首先激活JAK,然后再活化与之相结合的STAT1和STAT3,从而引起iNOS诱生型一氧化氮表达增强而诱发炎症反应,而IFN在诱导细胞的抗病毒和抗生长反应中也起关键作用。IFN可正向调节SOCS的表达,但是SOCS的过度表达又可以抑制IFN受体的磷酸化及STAT1、STAT3的活化。
Suppressors of eytokine signaling (SOCS) can be generated by the stimulation of eytokines through the signal activation of JAK/STAT pathway, and can later restrain the signal transduction of cytokines. Therefore SOCS is regarded as partial classic negative feedback loop. Interferon (IFN) are cytokines secreted by helper T cell and natural killer cells, which play roles in immune regulation. During inflammato- ry reaction, IFN activates JAK firstly and then activates STAT1 and STAT3 which combine to JAK. The phosphorylated STAT strengthens the expression of iNOS and induces inflammatory reaction. IFN plays an important role in antivirus and anti - growth responses. IFN can induce the expression of SOCS, but over - expression of SOCS will restrain the phosphorylation of IFN receptor and STAT1 or STAT3. Here we summarize the influence of SOCS on the activation of JAK/STAT to the signal transduction of IFN.
出处
《国际免疫学杂志》
CAS
2008年第4期311-313,共3页
International Journal of Immunology
关键词
SOCS
IFN
JAK/STAT信号传导通路
Suppressors of cytokine signaling
Interferon
Janus Kinase/signal transducers and activators of transcription