Activation of the NLRP3 inflammasome by proteins that signal for Necroptosis

Tae Bong Kang, Seung Hoon Yang, Beata Toth, Andrew Kovalenko, David Wallach

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

43 Scopus citations

Abstract

Necroptosis - a form of programmed necrotic cell death - and its resulting release of damage-associated molecular patterns (DAMPs) are believed to participate in the triggering of inflammatory processes. To assess the relative contribution of this cell death mode to inflammation, we need to know what other cellular effects can be exerted by molecules shown to trigger necrotic death, and the extent to which those effects might themselves contribute to inflammation. Here, we describe the technical approaches that have been applied to assess the impact of the main signaling molecules known to mediate activation of necroptosis upon generation of inflammatory cytokines in LPS-treated mouse bone marrow-derived dendritic cells. The findings obtained by this assessment indicated that signaling molecules known to initiate necroptosis can also initiate activation of the NLRP3 inflammasome, thereby inducing inflammation independently of cell death by triggering the generation of proinflammatory cytokines such as IL-1β.

Original languageEnglish
Title of host publicationRegulated Cell Death Part B - Necroptotic, Autophagic and other Non-apoptotic Mechanisms
PublisherAcademic Press Inc.
Pages67-81
Number of pages15
ISBN (Print)9780128014301
DOIs
StatePublished - 2014

Publication series

NameMethods in Enzymology
Volume545
ISSN (Print)0076-6879
ISSN (Electronic)1557-7988

Keywords

  • Caspase-8
  • DAMP
  • IL-1β
  • Inflammasome
  • Inflammation
  • MLKL
  • NLRP3
  • Necroptosis
  • Necrosis
  • RIPK3

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