Abdelaziz Dalia H A, Khalil Hany, Cormet-Boyaka Estelle, Amer Amal O
Department of Biochemistry and Molecular Biology, Faculty of Pharmacy, Helwan University, Cairo, Egypt.
Immunol Rev. 2015 May;265(1):194-204. doi: 10.1111/imr.12288.
Autophagy is originally described as the main catabolic pathway responsible for maintaining intracellular nutritional homeostasis that involves the formation of a unique vacuole, the autophagosome, and the interaction with the endosome-lysosome pathways. This conserved machinery plays a key role in immune-protection against different invaders, including pathogenic bacteria, intracellular parasites, and some viruses like herpes simplex and hepatitis C virus. Importantly, autophagy is linked to a number of human diseases and disorders including neurodegenerative disease, Crohn's disease, type II diabetes, tumorigenesis, cardiomyopathy, and fatty liver disease. On the other hand, inflammasomes are multiprotein platforms stimulated upon several environmental conditions and microbial infection. Once assembled, the inflammasomes mediate the maturation of pro-inflammatory cytokines and promote phagosome-lysosome fusion to sustain an innate immune response. The intersections between autophagy and inflammasome have been observed in various diseases and microbial infections. This review highlights the molecular aspects involved in autophagy and inflammasome interactions during different medical conditions and microbial infections.
自噬最初被描述为负责维持细胞内营养稳态的主要分解代谢途径，它涉及一种独特的液泡即自噬体的形成，以及与内体 - 溶酶体途径的相互作用。这种保守机制在针对不同入侵者的免疫保护中发挥关键作用，这些入侵者包括病原菌、细胞内寄生虫以及一些病毒，如单纯疱疹病毒和丙型肝炎病毒。重要的是，自噬与许多人类疾病和病症相关，包括神经退行性疾病、克罗恩病、II型糖尿病、肿瘤发生、心肌病和脂肪肝疾病。另一方面，炎性小体是在多种环境条件和微生物感染时被激活的多蛋白平台。一旦组装完成，炎性小体介导促炎细胞因子的成熟，并促进吞噬体 - 溶酶体融合以维持先天免疫反应。在各种疾病和微生物感染中都观察到了自噬与炎性小体之间的交叉。本综述重点介绍了在不同医学状况和微生物感染期间自噬与炎性小体相互作用所涉及的分子层面。
