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Regulation of inflammasomes by autophagy

机译:通过自噬调节炎症小体

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Inflammasomes detect pathogen-associated molecular patterns to induce inflammatory innate immune responses and play a key role in host defense against infectious agents. However, inflammasomes are often wrongly activated by metabolites, amyloids, and environmental irritants. This induces massive inflammation, causing severe tissue damage, and results in the development of inflammatory diseases. Hence cellular machineries regulating both "activation'' and "inactivation'' of inflammasomes are definitely important. Recent studies have shown that autophagy, an intracellular degradation system associated with maintenance of cellular homeostasis, plays a key role in inflammasome inactivation. Notably, autophagy deficiency caused by gene mutation disrupts organelle elimination and thus induces aberrant activation of inflammasomes, leading to severe tissue damage. Here we review recent findings regarding the involvement of autophagy in the regulation of inflammasome activation and development of inflammatory disorders.
机译:炎症小体检测与病原体相关的分子模式,以诱导炎症性先天免疫反应,并在宿主抵抗传染原的防御中发挥关键作用。但是,炎症小体通常被代谢物,淀粉样蛋白和环境刺激物错误地激活。这引起大量炎症,导致严重的组织损伤,并导致发炎性疾病的发展。因此,调节炎性小体的“活化”和“失活”的细胞机制绝对重要。最近的研究表明,自噬是一种与维持细胞稳态有关的细胞内降解系统,在炎症小体失活中起关键作用。值得注意的是,由基因突变引起的自噬缺陷破坏了细胞器的消除,从而引起了炎性体的异常激活,从而导致严重的组织损伤。在这里,我们回顾了有关自噬参与炎性体激活和炎症性疾病发展调控的最新发现。

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