Immune Regulation Research Group, School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland.
Immunol Cell Biol. 2013 Mar;91(3):250-8. doi: 10.1038/icb.2012.82. Epub 2013 Jan 15.
Autophagy is a cellular mechanism for the sequestration and degradation of intracellular pathogens and compromised organelles, particularly damaged mitochondria. Autophagy also clears other cellular components, such as inflammasomes and cytokines, thus providing an important means of regulating inflammation. Defects in autophagy have been found by genetic association studies to confer susceptibility to several autoimmune and inflammatory disorders, particularly inflammatory bowel disease. Thus, the manipulation of autophagy in disease situations is of growing interest for therapeutic targeting; however, the involvement of autophagy in cellular homoeostasis, in normal immune function and in inflammation is manifold. An appreciation of the intricacies of the contributions of this process to inflammation, and how these are altered by various immune and environmental stimuli, is essential for the understanding and interpretation of studies of inflammation and the design of therapeutics exploiting the manipulation of autophagy. This review focuses on the known roles of autophagy in the induction and maintenance of inflammation and on its role in the aetiology and regulation of inflammatory and autoimmune disorders.
自噬是一种细胞机制，用于隔离和降解细胞内病原体和受损细胞器，特别是受损的线粒体。自噬还可以清除其他细胞成分，如炎性体和细胞因子，从而提供一种重要的炎症调节手段。遗传关联研究发现，自噬缺陷使几种自身免疫和炎症性疾病（特别是炎症性肠病）易感性增加。因此，在疾病情况下操纵自噬对于治疗靶点的选择越来越受到关注；然而，自噬在细胞内稳态、正常免疫功能和炎症中的作用是多方面的。了解该过程对炎症的贡献的复杂性，以及各种免疫和环境刺激如何改变这些贡献，对于理解和解释炎症研究以及利用自噬操纵设计治疗方法至关重要。这篇综述重点介绍了自噬在炎症的诱导和维持中的已知作用，以及自噬在炎症性和自身免疫性疾病的发病机制和调节中的作用。
