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Switching Off Key Signaling Survival Molecules to Switch On the Resolution of Inflammation

机译:关闭关键的信号转导生存分子以打开炎症的解决方案

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摘要

Inflammation is a physiological response of the immune system to injury or infection but may become chronic. In general, inflammation is self-limiting and resolves by activating a termination program named resolution of inflammation. It has been argued that unresolved inflammation may be the basis of a variety of chronic inflammatory diseases. Resolution of inflammation is an active process that is fine-tuned by the production of proresolving mediators and the shutdown of intracellular signaling molecules associated with cytokine production and leukocyte survival. Apoptosis of leukocytes (especially granulocytes) is a key element in the resolution of inflammation and several signaling molecules are thought to be involved in this process. Here, we explore key signaling molecules and some mediators that are crucial regulators of leukocyte survival in vivo and that may be targeted for therapeutic purposes in the context of chronic inflammatory diseases.
机译:炎症是免疫系统对损伤或感染的生理反应,但可能会变为慢性。通常,炎症是自限性的,可通过激活名为炎症消退的终止程序来解决。有人认为,未解决的炎症可能是多种慢性炎症疾病的基础。炎症的消除是一个活跃的过程,可通过产生超分辨介体以及关闭与细胞因子产生和白细胞存活相关的细胞内信号分子来进行微调。白细胞(特别是粒细胞)的凋亡是解决炎症的关键因素,并且认为一些信号分子参与该过程。在这里,我们探索关键信号分子和一些介质,它们是体内白细胞存活的关键调节剂,在慢性炎症性疾病的治疗中可能靶向治疗。

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