TNF and ROS Crosstal in Inflammation

被引:789
作者
Blaser, Heiko [1 ]
Dostert, Catherine [2 ]
Mak, Tak W. [1 ,3 ,4 ]
Brenner, Dirk [2 ,5 ,6 ]
机构
[1] Univ Hlth Network, Campbell Family Canc Res Inst, Ontario Canc Inst, Toronto, ON, Canada
[2] Luxembourg Inst Hlth, Dept Infect & Immun Expt & Mol Immunol, 29 Rue Henri Koch, L-4354 Esch Sur Alzette, Luxembourg
[3] Univ Toronto, Dept Immunol, Toronto, ON, Canada
[4] Univ Toronto, Fac Med, Dept Med Biophys, Toronto, ON, Canada
[5] Univ Southern Denmark, Odense Univ Hosp, Dept Dermatol, ORCA, Odense, Denmark
[6] Univ Southern Denmark, Odense Univ Hosp, Allergy Ctr, ORCA, Odense, Denmark
基金
加拿大健康研究院;
关键词
TUMOR-NECROSIS-FACTOR; NF-KAPPA-B; OXYGEN SPECIES GENERATION; NECROTIC CELL-DEATH; ALPHA-INDUCED APOPTOSIS; REACTIVE OXYGEN; NITRIC-OXIDE; NADPH OXIDASE; OXIDATIVE STRESS; INDUCED NECROPTOSIS;
D O I
10.1016/j.tcb.2015.12.002
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Tumor necrosis factor (TNF) is tremendously important for mammalian immunity and cellular homeostasis. The role of TNF as a master regulator in balancing cell survival, apoptosis and necroptosis has been extensively studied in various cell types and tissues. Although these findings have revealed much about the direct impact of TNF on the regulation of NF-kappa B and JNK, there is now rising interest in understanding the emerging function of TNF as a regulator of the generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS). In this review we summarize work aimed at defining the role of TNF in the control of ROS/RNS signaling that influences innate immune cells under both physiological and inflammatory conditions.
引用
收藏
页码:249 / 261
页数:13
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