炎性小体激活与细胞焦亡的研究进展  

Research progress on inflammasome activation and pyroptosis

作　　者：杨斯迪[1] 邓奇峰[1] 黄瑞[1] 吴淑燕[1] 

机构地区：[1]苏州大学医学部基础医学与生物科学学院,苏州215123

出　　处：《微生物与感染》2017年第3期192-196,共5页Journal of Microbes and Infections

摘　　要：细胞焦亡是一种依赖天冬氨酸特异性半胱氨酸蛋白酶1(cysteinyl aspartate specific proteinase 1,caspase-1)/caspase-11的程序性细胞死亡方式。炎性小体的激活在细胞焦亡过程中扮演重要角色。当病原体入侵时,核苷酸结合寡聚化结构域样受体(nucleotide-binding oligomerization domain-like receptor,NLR)和黑色素瘤缺乏因子2(absent in melanoma 2,AIM2)等胞内模式识别受体(pattern recognition receptor,PRR)与相应配体结合,导致炎性小体多蛋白复合物组装和caspase-1/caspase-11激活,进而诱导细胞焦亡发生。深入研究炎性小体激活和细胞焦亡的相关机制,对认识炎症性疾病的发生发展非常重要。本文就炎性小体激活与细胞焦亡的研究进展进行综述。Pyroptosis is a new form of programmed cell death depending on cysteinyl aspartate specific proteinase 1 Ccaspase-1）. Inflammasome plays a significant role in regulating pyroptosis. Intracellular pattern recognition proteins such as nucleotide-binding oligomerization domain-like receptor （NLR） and absent in melanoma 2 （AIM2） act to their ligands and promote the assembly of inflammasome as well as the activation of caspase-l/caspase-11, then induce pyroptosis. The in-depth research on the mechanisms and correlation between pyroptosis and inflammasome contributes to the understanding of the occurrence and development of pyroptosis-related inflammatory diseases.

关 键 词：细胞焦亡 炎性小体 CASPASE-1 Caspase-11 

分 类 号：R363[医药卫生—病理学]