Journal
JOURNAL OF IMMUNOLOGY
Volume 192, Issue 5, Pages 2019-2026Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1302426
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Funding
- National Institutes of Health [R01 AI030363, AI020211, T32GM008169, OD012198]
- Achievement Rewards for College Scientists Fellowship
- University of Texas at Austin
- Cancer Prevention Research Institute of Texas
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Programmed necrosis mediated by receptor interacting protein kinase (RIP) 3 (also called RIPK3) has emerged as an alternate death pathway triggered by TNF family death receptors, pathogen sensors, IFNRs, Ag-specific TCR activation, and genotoxic stress. Necrosis leads to cell leakage and acts as a trap door, eliminating cells that cannot die by apoptosis because of the elaboration of pathogen-encoded caspase inhibitors. Necrotic signaling requires RIP3 binding to one of three partners-RIP1, DAI, or TRIF-via a common RIP homotypic interaction motif. Once activated, RIP3 kinase targets the pseudokinase mixed lineage kinase domain-like to drive cell lysis. Although necrotic and apoptotic death can enhance T cell cross-priming during infection, mice that lack these extrinsic programmed cell death pathways are able to produce Ag-specific T cells and control viral infection. The entwined relationship of apoptosis and necrosis evolved in response to pathogen-encoded suppressors to support host defense and contribute to inflammation.
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