[en] 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-κB 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.
Disciplines :
Immunologie & maladie infectieuse
Auteur, co-auteur :
Blaser, Heiko; The Campbell Family Cancer Research Institute, Ontario Cancer Institute, University Health Network, Toronto, Ontario, Canada
Dostert, Catherine; Department of Infection and Immunity, Experimental and Molecular Immunology, Luxembourg Institute of Health, 29, rue Henri Koch, 4354 Esch-sur-Alzette, Luxembourg
Mak, Tak W; The Campbell Family Cancer Research Institute, Ontario Cancer Institute, University Health Network, Toronto, Ontario, Canada, Department of Immunology, University of Toronto, Toronto, Ontario, Canada, Department of Medical Biophysics, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada
BRENNER, Dirk ; University of Luxembourg > Luxembourg Centre for Systems Biomedicine (LCSB) > Immunology and Genetics ; Department of Infection and Immunity, Experimental and Molecular Immunology, Luxembourg Institute of Health, 29, rue Henri Koch, 4354 Esch-sur-Alzette, Luxembourg, Odense Research Center for Anaphylaxis (ORCA), Department of Dermatology and Allergy Center, Odense University Hospital, University of Southern Denmark, Odense, Denmark. Electronic address: dirk.brenner@lih.lu
The authors thank M. Saunders for excellent scientific editing, K. Weger for the contribution of the glossary and research assistance, and M. Brenner for general support. H.B. is funded by a Canadian Institutes of Health Research (CIHR) S2B award (141816), and D.B. is funded by the ATTRACT Programme and a CORE grant (C15/BM/10355103) of the National Research Fund Luxembourg (FNR).
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