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Autophagy shapes inflammation.

机译:自噬会影响炎症。

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Autophagy is a basic cell biological process ongoing under physiologic circumstances in almost all cell types of the human organism and upregulated by various stress conditions including those leading to inflammation. Since autophagy affects the effector cells of innate and adaptive immunity mediating the inflammatory response, its activity in these cells influences the antimicrobial response, the development of an effective cognate immune defense, and the course of the normal sterile inflammatory reactions. The level of autophagic activity may determine whether tissue cells die by apoptosis, necrosis, or through autophagy, and, as a consequence, whether the clearance of these dying cells is a silent process or results in an inflammatory response. Loss or decreased autophagy may lead to necrotic death that can initiate an inflammatory reaction in phagocytes through their surface and cytosolic receptors. Engulfment of certain cells dying through autophagy can activate the inflammasome. The intertwining regulatory connections between inflammation and immunity extend to pathologic conditions including chronic inflammatory diseases, autoimmunity and cancer.
机译:自噬是一种基本的细胞生物学过程,是在生理条件下在几乎所有人类细胞类型中进行的,并且受各种应激条件(包括导致炎症的应激条件)上调。由于自噬影响介导炎症反应的先天性和适应性免疫的效应细胞,因此其在这些细胞中的活性会影响抗菌反应,有效的同类免疫防御的发展以及正常的无菌炎症反应的进程。自噬活性的水平可以确定组织细胞是通过凋亡,坏死还是通过自噬而死亡,因此确定这些垂死细胞的清除是沉默过程还是导致炎症反应。自噬的丧失或减少可能会导致坏死性死亡,从而导致吞噬细胞通过其表面和胞质受体引起炎症反应。通过自噬死亡的某些细胞的吞噬可以激活炎症小体。炎症和免疫力之间相互交织的调节联系延伸到病理状况,包括慢性炎症性疾病,自身免疫性和癌症。

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