RIPK3: Beyond Necroptosis

Azia S Evans; Carolyn B Coyne

doi:10.1016/j.immuni.2018.12.031

RIPK3: Beyond Necroptosis

Immunity. 2019 Jan 15;50(1):1-3. doi: 10.1016/j.immuni.2018.12.031.

Authors

Azia S Evans¹, Carolyn B Coyne²

Affiliations

¹ Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; Center for Microbial Pathogenesis, UPMC Children's Hospital of Pittsburgh, Pittsburgh, PA, USA.
² Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; Center for Microbial Pathogenesis, UPMC Children's Hospital of Pittsburgh, Pittsburgh, PA, USA; R. K. Mellon Institute for Pediatric Research, UPMC Children's Hospital of Pittsburgh, Pittsburgh, PA 15219, USA. Electronic address: coynec2@pitt.edu.

PMID: 30650369
DOI: 10.1016/j.immuni.2018.12.031

Abstract

In this issue of Immunity, Daniels et al. (2019) demonstrate that RIPK3 signaling limits Zika virus (ZIKV) infection in the central nervous system independently of its function in necroptosis by promoting itaconate production in infected neurons, thereby revealing a neuron-specific mechanism of metabolite-mediated ZIKV control.

Publication types

Research Support, N.I.H., Extramural
Comment

MeSH terms

Antiviral Agents*
Apoptosis
Carboxy-Lyases
Humans
Necrosis
Neurons
Nucleotides
Proteins
Receptor-Interacting Protein Serine-Threonine Kinases
Zika Virus Infection*
Zika Virus*

Substances

Antiviral Agents
Nucleotides
Proteins
RIPK3 protein, human
Receptor-Interacting Protein Serine-Threonine Kinases
ACOD1 protein, human
Carboxy-Lyases