Journal
IMMUNITY
Volume 38, Issue 2, Pages 209-223Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2013.02.003
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Funding
- Fund for Scientific Research Flanders (FWO-Vlaanderen) [G.0728.10, 3G067512, 3G060713, 3G0A5413]
- FWO-Vlaanderen [31507110]
- Emmanuel van der Schueren scholarship from the Flemish league against cancer
- European grants (FP6 ApopTrain, FP7 EC RTD Integrated Project, Apo-Sys, Euregional PACT II) [MRTNCT-035624, FP7-200767]
- Belgian grants (Interuniversity Attraction Poles) [IAP 6/18, IAP 7/32]
- Flemish grants (Research Foundation Flanders) [FWO G.0875.11, FWO G.0973.11, FWO G.0A45.12N]
- Ghent University grants (MRP, GROUP-ID consortium)
- Flanders Institute for Biotechnology (VIB)
- Foundation against Cancer [F94]
- Methusalem grant from the Flemish Government [BOF09/01M00709]
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Regulated necrosis, termed necroptosis, is negatively regulated by caspase-8 and is dependent on the kinase activity of RIPK1 and RIPK3. Necroptosis leads to rapid plasma membrane permeabilization and to the release of cell contents and exposure of damage-associated molecular patterns (DAMPs). We are only beginning to identify the necroptotic DAMPs, their modifications, and their potential role in the regulation of inflammation. In this review, we discuss the physiological relevance of necroptosis and its role in the modulation of inflammation. For example, during viral infection, RIPK3-mediated necroptosis acts as a backup mechanism to clear pathogens. Necroptosis is also involved in apparently immunologically silent maintenance of T cell homeostasis. In contrast, the induction of necroptosis in skin, intestine, systemic inflammatory response syndrome, and ischemia reperfusion injury provoke a strong inflammatory response, which might be triggered by emission of DAMPs from necroptotic cells, showing the detrimental side of necroptosis.
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