RIPK3-driven cell death during virus infections

Jason W. Upton, Maria Shubina, Siddharth Balachandran

Research output: Contribution to journalReview articlepeer-review

48 Scopus citations

Abstract

The programmed self-destruction of infected cells is a powerful antimicrobial strategy in metazoans. For decades, apoptosis represented the dominant mechanism by which the virus-infected cell was thought to undergo programmed cell death. More recently, however, new mechanisms of cell death have been described that are also key to host defense. One such mechanism in vertebrates is programmed necrosis, or “necroptosis”, driven by receptor-interacting protein kinase 3 (RIPK3). Once activated by innate immune stimuli, including virus infections, RIPK3 phosphorylates the mixed lineage kinase domain-like protein (MLKL), which then disrupts cellular membranes to effect necroptosis. Emerging evidence demonstrates that RIPK3 can also mediate apoptosis and regulate inflammasomes. Here, we review studies on the mechanisms by which viruses activate RIPK3 and the pathways engaged by RIPK3 that drive cell death.

Original languageEnglish
Pages (from-to)90-101
Number of pages12
JournalImmunological Reviews
Volume277
Issue number1
DOIs
StatePublished - Apr 2017

Keywords

  • Animals
  • Apoptosis
  • Humans
  • Immunity, Innate
  • Inflammasomes/metabolism
  • Necrosis
  • Protein Kinases/metabolism
  • Receptor-Interacting Protein Serine-Threonine Kinases/metabolism
  • Virus Diseases/immunology
  • Viruses/immunology

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