Switching off key signaling survival molecules to switch on the resolution of inflammation.
Switching off key signaling survival molecules to switch on the resolution of inflammation.
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DOI：
10.1155/2014/829851
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发表时间：
2014
影响因子：
4.6
通讯作者：
Pinho V
中科院分区：
文献类型：
--
作者：
Perez DA;Vago JP;Athayde RM;Reis AC;Teixeira MM;Sousa LP;Pinho V
炎症是免疫系统对损伤或感染的一种生理反应，但也可能成为慢性反应。一般来说，炎症是自我限制的，通过激活一个名为炎症消退的终止程序来解决。人们一直认为，未解决的炎症可能是各种慢性炎症性疾病的基础。炎症的消退是一个活跃的过程，由促炎性介质的产生和与细胞因子产生和白细胞存活相关的细胞内信号分子的关闭进行微调。白细胞（尤其是粒细胞）的凋亡是炎症消退的关键因素，一些信号分子被认为参与了这一过程。在这里，我们探索了关键的信号分子和一些介质，它们是体内白细胞存活的关键调节因子，可能是慢性炎症性疾病治疗目的的靶标。
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.