摘要
炎性小体是胞质内的一组多蛋白复合体,一方面它能调节半胱氨酸天冬氨酸特异蛋白酶1的活化,促进IL-1β和IL-18成熟与分泌,引起炎性反应;另一方面可以引起细胞焦亡。NLRC4炎性小体的主要信号途径为:激活物(如细菌鞭毛蛋白)、感应蛋白(NAIP)、核效应蛋白(NLRC4)、连接蛋白(ASC)、效应蛋白。NLRC4活化的主要调控机制是配体结合机制和磷酸化作用。NLRC4是肠道免疫的重要组成成分,可抵御多种病原体,并与多种人类疾病相关,如自身炎性疾病、糖尿病肾病、胸腺癌等。
Inflammasomes are cytosolic multiprotein complexes that can regulate the activation of caspase-1, promote the maturation and secretion of IL-1β and IL-18,and lead to inflammation,meanwhile initiate pyroptosis. The classic illustration of the NLRC4 inflammasome paradigm is: trigger(cytosolic flagellin), sensor(NAIP), nucleator(NLRC4), adaptor(ASC), and effector(caspase-1). The main regulatory mechanisms of NLRC4 activation are ligand binding and phosphorylation. NLRC4 is a critical component of intestinal immune system and defense against different pathogens. In addition,NLRC4 related to a variety of human diseases: such as autoinflammatory diseases, diabetic nephropathy, thymic cancer.
作者
俞源源
刘映红
袁芳
YU Yuan-yuan;LIU Ying-hong;YUAN Fang(Hunan Provincial Key Laboratory of Kidney Diseases and Blood Purification,the Second Xiangya Hospital,Xiangya Medical College,Central South University,Changsha 410011,China)
出处
《基础医学与临床》
CSCD
2019年第4期564-568,共5页
Basic and Clinical Medicine
基金
国家自然科学基金(81770730)
湖南省自然科学基金(2017JJ2352)