ZBP1/DAI is an innate sensor of influenza virus triggering the NLRP3 inflammasome and programmed cell death pathways
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ZBP1 activates the NLRP3 inflammasome and programmed cell death.
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Multiple components of molecular machinery for necroptosis-including ZBP1, RIPK3, MLKL, and TNFR1 (mainly via NF-κB)-impinge on control of inflammasome, a supramolecular platform for activation of CASP1 and consequent secretion of mature IL1B and IL18.
“Importantly, multiple components of the molecular machinery for necroptosis—including ZBP1, RIPK3, MLKL, and TNFR1 (mainly via NF-κB)—impinge on the control of the so-called “inflammasome”, a supramolecular platform for the activation of CASP1 and consequent secretion of mature interleukin 1 beta (IL1B; best known as IL-1β) and IL18 [524–529].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [525]
Type I IFN and IFNG contribute to pyroptosis by promoting TLR7, CGAS, STING, RIG-I, or MAVS signaling upon bacterial or viral infection.
“(2) TLR7, cyclic GMP-AMP synthase (CGAS), transmembrane protein 173 (TMEM173; best known as STING), DExD/H-box helicase 58 (DDX58; best known as RIG-I), or mitochondrial antiviral signaling protein (MAVS) signaling upon bacterial or viral infection [525, 645]”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [525]
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- Authors
- Kuriakose, T., Man, S. M., Subbarao Malireddi, R. K., Karki, R., Kesavardhana, S., Place, D. E., Neale, G., Vogel, P., & Kanneganti, T.-D.
- Affiliations
- St. Jude Children's Research Hospital (US)
- Department of Immunology, St. Jude Children’s Research Hospital, Memphis, TN 38105, USA.
- Corresponding author
- Kanneganti, Thirumala-Devi
- ORCID
- Venue
- Science Immunology
- Published
- 2016-08-05
- Volume
- 1
- Issue
- 2
- ISSN
- 2470-9468 (ISSN-L)
- PMC
- PMC5131924
- OpenAlex
- W2507605260
- Cited by
- 818
- References
- 48
- Citations by year
- 2026: 96 · 2025: 161 · 2024: 115 · 2023: 105 · 2022: 75 · 2021: 75 · 2020: 77 · 2019: 38 · 2018: 35 · 2017: 36 · 2016: 5
- FWCI
- 23.05
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science Immunology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- ANU Open Research (Australian National University) (submittedVersion)
- Seoul National University Open Repository (Seoul National University) (submittedVersion)
- Funders
- National Cancer Institute (R01CA163507, P30CA021765)
- National Institute of Allergy and Infectious Diseases (R01AI101935, R37AI101935, R01AI124346)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR056296)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- ZBP1, DAI, influenza A virus, innate immune recognition, NLRP3 inflammasome, RIPK1, RIPK3, caspase-8, necroptosis, pyroptosis, apoptosis, interferon-induced proteins, viral pathogenesis
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