摘要
炎症小体作为重要的固有免疫成分，可通过外源性病原体相关分子模式（PAMPs）和内源性损伤相关分子模式（DAMPs）激活。炎症小体的激活涉及蛋白复合物的形成和寡聚化，引起caspase-1激活，导致促炎因子IL-1β和IL-18释放。目前，自噬被认为是炎症小体的主要调节器。细胞自噬参与细胞稳态，清除损伤的细胞器（例如线粒体）和胞内病原体的重要的细胞内过程。深入研究炎症小体与自噬相互调控机制，对认识炎症性疾病的发生发展非常重要。
Inflammasome, as an important innate immune component, can be activated by exogenous pathogen-associated molecular patterns （PAMPs） and endogenous damage related molecular patterns （DAMPs）. Activation of the inflammasome involves the formation and oligomerisation of protein complexes, triggering the activation of caspase-1, leading to the release of proinflammatory cytokines interleukin 1β （IL-1β） and IL-18. At present, autophagy is considered as the main regulator of the inflammasome. Autophagy is involved in cellular homeostasis, an important intracellular processes that removes damaged organelles （such as mitochondria） and intracellular pathogens. Further study in the mechanism of mutual regulation inflammasome and autophagy is very important for understanding the occurrence and development of inflammatory diseases.
作者
吴玲玲
于化鹏
陈丽嫦
曾冠盛
Wu Lingling;Yu Huapeng;Chen Lichang;Zeng Guansheng(Department of Respiratory Medicine,Zhujiang Hospital,Southern Medical University,Guangzhou 510280,China)
出处
《国际呼吸杂志》
2018年第13期1011-1015,共5页
International Journal of Respiration
基金
广东省科技计划项目（2014A020212395）
