RIPK3: Beyond Necroptosis

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 meta...

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Veröffentlicht in:	Immunity (Cambridge, Mass.) Mass.), 2019-01, Vol.50 (1), p.1-3
Hauptverfasser:	Evans, Azia S., Coyne, Carolyn B.
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Antiviral Agents Apoptosis Brain Carboxy-Lyases Central nervous system Genes Genotype & phenotype Humans Immunity Infections Kinases Metabolism Metabolites Necroptosis Necrosis Nervous system Neurons Nucleotides Proteins Receptor-Interacting Protein Serine-Threonine Kinases Vector-borne diseases Viral infections Viruses West Nile virus Zika Virus Zika Virus Infection
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Beschreibung
Zusammenfassung:	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. 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.
ISSN:	1074-7613 1097-4180
DOI:	10.1016/j.immuni.2018.12.031