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RIPK 3‐driven cell death during virus infections
Author(s) -
Upton Jason W.,
Shubina Maria,
Balachandran Siddharth
Publication year - 2017
Publication title -
immunological reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.839
H-Index - 223
eISSN - 1600-065X
pISSN - 0105-2896
DOI - 10.1111/imr.12539
Subject(s) - necroptosis , programmed cell death , biology , microbiology and biotechnology , ripk1 , apoptosis , innate immune system , protein kinase a , kinase , mechanism (biology) , immune system , immunology , genetics , philosophy , epistemology
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 ( RIPK 3). Once activated by innate immune stimuli, including virus infections, RIPK 3 phosphorylates the mixed lineage kinase domain‐like protein ( MLKL ), which then disrupts cellular membranes to effect necroptosis. Emerging evidence demonstrates that RIPK 3 can also mediate apoptosis and regulate inflammasomes. Here, we review studies on the mechanisms by which viruses activate RIPK 3 and the pathways engaged by RIPK 3 that drive cell death.