Immunology Research Centre, School of Biochemistry & Immunology, Trinity College Dublin, College Green, Dublin 2, Ireland.
Cytokine. 2011 Nov;56(2):140-4. doi: 10.1016/j.cyto.2011.08.022. Epub 2011 Sep 1.
Autophagy is a highly conserved homoeostatic mechanism for the lysosomal degradation of cytosolic constituents, including long-lived macromolecules, organelles and intracellular pathogens. Autophagosomes are formed in response to a number of environmental stimuli, including amino acid deprivation, but also by both host- and pathogen-derived molecules, including toll-like receptor ligands and cytokines. In particular, IFN-γ, TNF-α, IL-1, IL-2, IL-6 and TGF-β have been shown to induce autophagy, while IL-4, IL-10 and IL-13 are inhibitory. Moreover, autophagy can itself regulate the production and secretion of cytokines, including IL-1, IL-18, TNF-α, and Type I IFN. This review discusses the potentially pivotal roles of autophagy in the regulation of inflammation and the coordination of innate and adaptive immune responses.
自噬是一种高度保守的溶酶体降解细胞质成分的同源平衡机制，包括长寿命的大分子、细胞器和细胞内病原体。自噬体是在多种环境刺激下形成的，包括氨基酸剥夺，但也包括宿主和病原体来源的分子，包括 Toll 样受体配体和细胞因子。特别是，IFN-γ、TNF-α、IL-1、IL-2、IL-6 和 TGF-β已被证明能诱导自噬，而 IL-4、IL-10 和 IL-13 则具有抑制作用。此外，自噬本身可以调节细胞因子的产生和分泌，包括 IL-1、IL-18、TNF-α 和 I 型 IFN。这篇综述讨论了自噬在调节炎症和协调先天和适应性免疫反应方面的潜在关键作用。
