ArticleCell death & disease2021
Viral dosing of influenza A infection reveals involvement of RIPK3 and FADD, but not MLKL.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 27 citations in OpenAlex.
- Targeting MLKL-Driven Necroptosis: A Therapeutic Target in Inflammation and Host Defense.Biomolecules · 2026Review
- Dissecting Cell Death Pathways in Influenza A Virus Infection: Comparative Insights from Human Models.Viruses · 2026Review
- The cell death regulator c-FLIPJournal of molecular medicine (Berlin, Germany) · 2025Article
- Influenza a(H1N1) virus infection impairs syncytiotrophoblast functions by promoting ferroptosis through the TNF-α/ISG15/EGR1 axis.Virology journal · 2025Article
- ZBP1-driven cell death in severe influenza.Trends in microbiology · 2025Review
- Influenza-induced microRNA-155 expression is altered in extracellular vesicles derived from the COPD epithelium.Frontiers in cellular and infection microbiology · 2025Article
- Mechanistic Insights into Influenza A Virus-Induced Cell Death and Emerging Treatment Strategies.Veterinary sciences · 2024Review
- Influenza virus infection activates TAK1 to suppress RIPK3-independent apoptosis and RIPK1-dependent necroptosis.Cell communication and signaling : CCS · 2024Article
- Need for standardization of Influenza A virus-induced cell death in vivo to improve consistency of inter-laboratory research findings.Cell death discovery · 2024Review
- Interaction among inflammasome, PANoptosise, and innate immune cells in infection of influenza virus: Updated review.Immunity, inflammation and disease · 2023Review
- PANoptosome signaling and therapeutic implications in infection: central role for ZBP1 to activate the inflammasome and PANoptosis.Current opinion in immunology · 2023Review
- Cleavage of cFLIP restrains cell death during viral infection and tissue injury and favors tissue repair.Science advances · 2023Article
- Article
- Inflammatory cell death: how macrophages sense neighbouring cell infection and damage.Biochemical Society transactions · 2023Review
- MLKL post-translational modifications: road signs to infection, inflammation and unknown destinations.Cell death and differentiation · 2023Review
- Host A-to-I RNA editing signatures in intracellular bacterial and single-strand RNA viral infections.Frontiers in immunology · 2023Article
- Regulated necrosis, a proinflammatory cell death, potentially counteracts pathogenic infections.Cell death & disease · 2022Review
- Review
- Reduced protection of RIPK3-deficient mice against influenza by matrix protein 2 ectodomain targeted active and passive vaccination strategies.Cell death & disease · 2022Article
- Identification of Nifurtimox and Chrysin as Anti-Influenza Virus Agents by Clinical Transcriptome Signature Reversion.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RIPK3 was reported to play an important role in the protection against influenza A virus (IAV) in vivo. Here we show that the requirement of RIPK3 for protection against IAV infection in vivo is only apparent within a limited dose range of IAV challenge. We found that this protective outcome is independent from RIPK3 kinase activity and from MLKL. This shows that platform function of RIPK3 rather than its kinase activity is required for protection, suggesting that a RIPK3 function independent of necroptosis is implicated. In line with this finding, we show that FADD-dependent apoptosis has a crucial additional effect in protection against IAV infection. Altogether, we show that RIPK3 contributes to protection against IAV in a narrow challenge dose range by a mechanism that is independent of its kinase activity and its capacity to induce necroptosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.