锌指蛋白A20对Toll样受体信号途径的负反馈调控及其对机体的保护作用

Protective effects of feedback control on TLR signaling pathway by zinc finger protein A20

Toll样受体（TLR）能够识别病原体，并在病原体入侵机体的早期启动固有免疫，促进免疫细胞成熟分化及调节免疫应答，触发炎症反应。脂多糖（LPS）激活TLR4的信号转导通路后导致NF—κB和JNK／SAPK激活，使炎症因子大量表达，导致全身炎症反应和多器官功能衰竭的发生。A20作为一种NF—κB依赖性表达的胞质蛋自，对NF—κB活性有负反馈调控作用，参与了体内炎症反应的调节和凋亡抑制，对机体起到保护作用。

Toll-like receptors （TLRs） recognize pathogens and initiate innate immune responses at the early stage of virus invasion, promoting the maturation and differentiation of immune cells ,regulating immune responses, and triggering inflammatory responses. Lipopolysaeeharide （LPS） activates the TLR4 signaling pathways which result in the activation of NF-κB and JNK/SAPK and the expression of large amounts of inflammaory factors,leading to systemic inflammatory response and multiple organ failure. A20, a NF-κB-dependant cytosolic protein,via a negative feedback loop blocks NF--κB activation and participates in the regulation of inflammatory responses and the inhibition of apptosis; therefore, it provides protective effect on the body.