TY - JOUR
T1 - RIPK3-driven cell death during virus infections
AU - Upton, Jason W.
AU - Shubina, Maria
AU - Balachandran, Siddharth
N1 - Publisher Copyright:
© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
PY - 2017/4
Y1 - 2017/4
N2 - 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.
AB - 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.
KW - Animals
KW - Apoptosis
KW - Humans
KW - Immunity, Innate
KW - Inflammasomes/metabolism
KW - Necrosis
KW - Protein Kinases/metabolism
KW - Receptor-Interacting Protein Serine-Threonine Kinases/metabolism
KW - Virus Diseases/immunology
KW - Viruses/immunology
UR - http://www.scopus.com/inward/record.url?scp=85018978167&partnerID=8YFLogxK
UR - https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=purepublist2023&SrcAuth=WosAPI&KeyUT=WOS:000400377200007&DestLinkType=FullRecord&DestApp=WOS
U2 - 10.1111/imr.12539
DO - 10.1111/imr.12539
M3 - Review article
C2 - 28462524
SN - 0105-2896
VL - 277
SP - 90
EP - 101
JO - Immunological Reviews
JF - Immunological Reviews
IS - 1
ER -