S-nitrosylation/Denitrosylation and Apoptosis of Immune Cells

作     者：Shaojin Duan Chang Chen 

作者机构：Guang An Men Hospital China Academy of Chinese Medical SciencesBeijing 10053 China National Laboratory of Biomacromolecules Institute of BiophysicsChinese Academy of Sciences Beijing 100101 China 

出 版 物：《Cellular & Molecular Immunology》 (中国免疫学杂志（英文版）)

年 卷 期：2007年第4卷第5期

页      面：353-358页

核心收录：

学科分类：1001[医学-基础医学(可授医学、理学学位)] 100101[医学-人体解剖与组织胚胎学] 10[医学] 

基　　金：The work was supported by the National Basic Research Program of China (2006CB911000, 2006CB503900) the National Natural Science Foundation of China (30770512, 39770202) 

主　　题：immune cell nitric oxide apoptosis S-nitrosylation/denitrosylation switch host defense 

摘      要：Nitric oxide （NO） as an immunoregulatory molecule, predominantly depending on S-nitrosylation, acts as a versatile player that executes its regulation and signal transduction for exerting its multi-functions and pleiotropy. Apoptosis of immune cells is an intricate process coupled with positive/negative selection depending on integrated diverse endogenous and exogenous signals and functions to sustain homeostasis in the immune system. Here, the dual roles of NO depending on its concentration in apoptosis are reviewed, breeding up a switch mode in the apoptotic process. Following comments of different switches from apoptosis-death, a new finding of checkpoint （early fluorescence point） of GSNO-initiated thymocyte apoptosis and NOS-GSNOR double control are highlighted. Moreover, S-nitrosylation/denitrosylation, being as a redox switch, logically approaches to networks of metabolism itself and further accesses the neuroendicrine-immune-free radical network as a whole. Moreover, the host defense mediated by NO on pathogens, via protein S-nitrosylation are also discussed.