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Necroptosis suppresses inflammation via termination of TNF- or LPS-induced cytokine and chemokine production
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Journal Article
Necroptosis suppresses inflammation via termination of TNF- or LPS-induced cytokine and chemokine production
2015
Overview
TNF promotes a regulated form of necrosis, called necroptosis, upon inhibition of caspase activity in cells expressing RIPK3. Because necrosis is generally more pro-inflammatory than apoptosis, it is widely presumed that TNF-induced necroptosis may be detrimental
in vivo
due to excessive inflammation. However, because TNF is intrinsically highly pro-inflammatory, due to its ability to trigger the production of multiple cytokines and chemokines, rapid cell death via necroptosis may blunt rather than enhance TNF-induced inflammation. Here we show that TNF-induced necroptosis potently suppressed the production of multiple TNF-induced pro-inflammatory factors due to RIPK3-dependent cell death. Similarly, necroptosis also suppressed LPS-induced pro-inflammatory cytokine production. Consistent with these observations, supernatants from TNF-stimulated cells were more pro-inflammatory than those from TNF-induced necroptotic cells
in vivo
. Thus necroptosis attenuates TNF- and LPS-driven inflammation, which may benefit intracellular pathogens that evoke this mode of cell death by suppressing host immune responses.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 38
/ 82
/ Biomedical and Life Sciences
/ Humans
/ Lipopolysaccharides - pharmacology
/ Protein Kinases - metabolism
/ Receptor-Interacting Protein Serine-Threonine Kinases - genetics
/ Receptor-Interacting Protein Serine-Threonine Kinases - metabolism
/ Toll-Like Receptor 4 - genetics
