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10.1016/j.immuni.2022.01.003

http://scihub22266oqcxt.onion/10.1016/j.immuni.2022.01.003
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suck abstract from ncbi


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pmid35139355      Immunity 2022 ; 55 (3): 423-441.e9
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  • Interferon-gamma primes macrophages for pathogen ligand-induced killing via a caspase-8 and mitochondrial cell death pathway #MMPMID35139355
  • Simpson DS; Pang J; Weir A; Kong IY; Fritsch M; Rashidi M; Cooney JP; Davidson KC; Speir M; Djajawi TM; Hughes S; Mackiewicz L; Dayton M; Anderton H; Doerflinger M; Deng Y; Huang AS; Conos SA; Tye H; Chow SH; Rahman A; Norton RS; Naderer T; Nicholson SE; Burgio G; Man SM; Groom JR; Herold MJ; Hawkins ED; Lawlor KE; Strasser A; Silke J; Pellegrini M; Kashkar H; Feltham R; Vince JE
  • Immunity 2022[Mar]; 55 (3): 423-441.e9 PMID35139355show ga
  • Cell death plays an important role during pathogen infections. Here, we report that interferon-gamma (IFNgamma) sensitizes macrophages to Toll-like receptor (TLR)-induced death that requires macrophage-intrinsic death ligands and caspase-8 enzymatic activity, which trigger the mitochondrial apoptotic effectors, BAX and BAK. The pro-apoptotic caspase-8 substrate BID was dispensable for BAX and BAK activation. Instead, caspase-8 reduced pro-survival BCL-2 transcription and increased inducible nitric oxide synthase (iNOS), thus facilitating BAX and BAK signaling. IFNgamma-primed, TLR-induced macrophage killing required iNOS, which licensed apoptotic caspase-8 activity and reduced the BAX and BAK inhibitors, A1 and MCL-1. The deletion of iNOS or caspase-8 limited SARS-CoV-2-induced disease in mice, while caspase-8 caused lethality independent of iNOS in a model of hemophagocytic lymphohistiocytosis. These findings reveal that iNOS selectively licenses programmed cell death, which may explain how nitric oxide impacts disease severity in SARS-CoV-2 infection and other iNOS-associated inflammatory conditions.
  • |Animals[MESH]
  • |COVID-19/*immunology[MESH]
  • |Caspase 8/genetics/*metabolism[MESH]
  • |Cells, Cultured[MESH]
  • |Cytotoxicity, Immunologic[MESH]
  • |Humans[MESH]
  • |Interferon-gamma/genetics/*metabolism[MESH]
  • |Lymphohistiocytosis, Hemophagocytic/*immunology[MESH]
  • |Macrophage Activation[MESH]
  • |Macrophages/*immunology[MESH]
  • |Mice[MESH]
  • |Mice, Inbred C57BL[MESH]
  • |Mice, Knockout[MESH]
  • |Mitochondria/*metabolism[MESH]
  • |Nitric Oxide Synthase Type II/metabolism[MESH]
  • |Pathogen-Associated Molecular Pattern Molecules/immunology[MESH]
  • |SARS-CoV-2/*physiology[MESH]
  • |Signal Transduction[MESH]
  • |bcl-2 Homologous Antagonist-Killer Protein/genetics/metabolism[MESH]


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