ReviewJournal of immunology (Baltimore, Md. : 1950)2014
True grit: programmed necrosis in antiviral host defense, inflammation, and immunogenicity.
Review in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
53 citing papers in PubMed, 73 citations in OpenAlex.
- UL45 of Human Cytomegalovirus Promotes Macrophage Survival and Modulates RIPK3-Associated Cell Death.Viruses · 2026Article
- Z-Nucleic Acid-Binding Protein (ZBP)1 (DAI/DLM1) Regulation in Antiviral Cell Death Pathways.Pathogens (Basel, Switzerland) · 2026Review
- Review
- The RIPK3 Scaffold Regulates Lung Inflammation DuringAmerican journal of respiratory cell and molecular biology · 2023Article
- Cell death proteins in sepsis: key players and modern therapeutic approaches.Frontiers in immunology · 2023Review
- Outcomes of RIP Kinase Signaling During Neuroinvasive Viral Infection.Current topics in microbiology and immunology · 2023Review
- Programmed Necrosis in Host Defense.Current topics in microbiology and immunology · 2023Article
- Opposite Effects of Apoptotic and Necroptotic Cellular Pathways on Rotavirus Replication.Journal of virology · 2022Article
- The adaptation of SARS-CoV-2 to humans.Memorias do Instituto Oswaldo Cruz · 2022Article
- Z-RNA and the Flipside of the SARS Nsp13 Helicase: Is There a Role for Flipons in Coronavirus-Induced Pathology?Frontiers in immunology · 2022Article
- Role of Damage-Associated Molecular Pattern/Cell Death Pathways in Vaccine-Induced Immunity.Viruses · 2021Review
- The Antisocial Network: Cross Talk Between Cell Death Programs in Host Defense.Annual review of immunology · 2021Article
- Human NK cells: From development to effector functions.Innate immunity · 2021Review
- RIPK protein kinase family: Atypical lives of typical kinases.Seminars in cell & developmental biology · 2021Review
- Necroptosis restricts influenza A virus as a stand-alone cell death mechanism.The Journal of experimental medicine · 2020Article
- Article
- Knocking 'em Dead: Pore-Forming Proteins in Immune Defense.Annual review of immunology · 2020Review
- Benefits and Perils of Necroptosis in Influenza Virus Infection.Journal of virology · 2020Review
- Article
- Caspase-8 restricts natural killer cell accumulation during MCMV Infection.Medical microbiology and immunology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
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.
Indexed as
Identifiers
What OpenQuestion holds
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.