ArticleFrontiers in immunology2018
IFNAR2 Is Required for Anti-influenza Immunity and Alters Susceptibility to Post-influenza Bacterial Superinfections.
Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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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.
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Who cites it
34 citing papers in PubMed, 52 citations in OpenAlex.
- Strong, sustained type I IFN signaling acts cell intrinsically to impair IFNγ responses and cause tuberculosis susceptibility.Cell host & microbe · 2026Article
- Identifying severe COVID-19 risk variants modulating enhancer reporter activity in lung cells.PLoS genetics · 2026Article
- Strong sustained type I IFN signaling acts cell intrinsically to impair IFNγ responses and cause tuberculosis susceptibility.bioRxiv : the preprint server for biology · 2026Article
- Impact of IFITM3 rs12252 and IFNAR2 rs2236757 SNP polymorphisms on influenza virus infection outcomes in Moroccan patients.Molecular biology reports · 2025Article
- IFITM3-deficient mice as a model for testing influenza virus vaccines via the intramuscular route.Vaccine · 2025Article
- Epigenetic changes and serotype-specific responses of alveolar type II epithelial cells to Streptococcus pneumoniae in resolving influenza A virus infection.Cell communication and signaling : CCS · 2025Article
- IFN Receptor 2 Regulates TNF-α-Mediated Damaging Inflammation during Aspergillus Pulmonary Infection.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Review
- The Cytomegalovirus M35 Protein Directly Binds to the Interferon-β Enhancer and Modulates Transcription ofJournal of virology · 2023Article
- Autoantibodies are highly prevalent in non-SARS-CoV-2 respiratory infections and critical illness.JCI insight · 2023Article
- Exposing the Two Contrasting Faces of STAT2 in Inflammation.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2022Review
- Pathophysiology of Influenza D Virus Infection in Specific-Pathogen-Free Lambs with or without PriorViruses · 2022Article
- Life-threatening viral disease in a novel form of autosomal recessive IFNAR2 deficiency in the Arctic.The Journal of experimental medicine · 2022Article
- Oncolytic Vaccinia Virus HarboringMarine drugs · 2022Article
- Pleiotropic Effects of Influenza H1, H3, and B Baloxavir-Resistant Substitutions on Replication, Sensitivity to Baloxavir, and Interferon Expression.Antimicrobial agents and chemotherapy · 2022Article
- Identification of Nifurtimox and Chrysin as Anti-Influenza Virus Agents by Clinical Transcriptome Signature Reversion.International journal of molecular sciences · 2022Article
- Review
- Integrative genomic analyses identify susceptibility genes underlying COVID-19 hospitalization.Nature communications · 2021Article
- Integrative genomics analysis reveals a 21q22.11 locus contributing risk to COVID-19.Human molecular genetics · 2021Article
- Viral infections in humans and mice with genetic deficiencies of the type I IFN response pathway.European journal of immunology · 2021Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Influenza virus infections particularly when followed by bacterial superinfections (BSI) result in significant morbidities and mortalities especially during influenza pandemics. Type I interferons (IFNs) regulate both anti-influenza immunity and host susceptibility to subsequent BSIs. These type I IFNs consisting of, among others, 14 IFN-α's and a single IFN-β, are recognized by and signal through the heterodimeric type I IFN receptor (IFNAR) comprised of IFNAR1 and IFNAR2. However, the individual receptor subunits can bind IFN-β or IFN-α's independently of each other and induce distinct signaling. The role of type I IFN signaling in regulating host susceptibility to both viral infections and BSI has been only examined with respect to IFNAR1 deficiency. Here, we demonstrate that despite some redundancies, IFNAR1 and IFNAR2 have distinct roles in regulating both anti-influenza A virus (IAV) immunity and in shaping host susceptibility to subsequent BSI caused by
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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.