ArticlePLoS pathogens2011
Type I interferon signaling regulates Ly6C(hi) monocytes and neutrophils during acute viral pneumonia in mice.
Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 147 papers.
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Who cites it
147 citing papers in PubMed, 209 citations in OpenAlex.
- Type I IFN coordinates resistance and tolerance against Zika virus disease by inducing NK cell recruitment and limiting neutrophil-driven neuropathology in the brain.Brain, behavior, & immunity - health · 2026Article
- Spatiotemporal heterologous vaccination relies on type I interferons at priming to enhance mucosal immunity.EMBO molecular medicine · 2026Article
- Alveolar Macrophages: Development, Respiratory Homeostasis, Signal Pathways, Diseases, and Therapeutic Opportunities.MedComm · 2026Review
- Diabetes Mellitus with Influenza Virus and Subsequent Bacterial Infection: Triple Pathological Interactions and Challenges.International journal of molecular sciences · 2026Review
- Deciphering interferon functions in avian influenza using receptor knockout models in the natural host.eLife · 2026Article
- Article
- Influenza hijacks myeloid cells to inflict type-I interferon-fueled damage in the heart.Immunity · 2026Article
- Ubiquitin E3 ligase MARCH10 targets influenza hemagglutinin for ubiquitination.Cellular signalling · 2025Article
- Age-associated immune dysregulation and B cell dysfunction drive severe outcomes in SFTSV infection.PLoS pathogens · 2025Article
- Type I Interferon Targets Alveolar Macrophages to Promote Bacterial Pneumonia after Viral Infection.American journal of respiratory cell and molecular biology · 2025Article
- Systemic inflammation impairs myelopoiesis and interferon type I responses in humans.Nature immunology · 2025Article
- Quercetin-3-Methyl Ether Induces Early Apoptosis to Overcome HRV1B Immune Evasion, Suppress Viral Replication, and Mitigate Inflammatory Pathogenesis.Biomolecules & therapeutics · 2025Article
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- Type I interferons in bacterial diseases: myeloid cells at the crossroads of protection and pathology.Frontiers in immunology · 2025Review
- Mathematical Model of Influenza Infection Suggests JAK-STAT Activity Drives Severe Pathologies in Juvenile Mice.Frontiers in applied mathematics and statistics · 2025Article
- Diphenyl pyridine intervention improvesFrontiers in genetics · 2025Article
- Integrated network pharmacology andFrontiers in molecular biosciences · 2025Article
- Nasal virus infection induces asthma exacerbation through B-cell-dependent recruitment of inflammatory monocytes.International forum of allergy & rhinology · 2024Article
- Newly isolated Lactobacillus paracasei strain modulates lung immunity and improves the capacity to cope with influenza virus infection.Microbiome · 2023Article
- Respiratory viral infection and resolution of inflammation: Roles for specialized pro-resolving mediators.Experimental biology and medicine (Maywood, N.J.) · 2023Review
87 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type I interferon (IFN-I) plays a critical role in the homeostasis of hematopoietic stem cells and influences neutrophil influx to the site of inflammation. IFN-I receptor knockout (Ifnar1⁻/⁻) mice develop significant defects in the infiltration of Ly6C(hi) monocytes in the lung after influenza infection (A/PR/8/34, H1N1). Ly6C(hi) monocytes of wild-type (WT) mice are the main producers of MCP-1 while the alternatively generated Ly6C(int) monocytes of Ifnar1⁻/⁻ mice mainly produce KC for neutrophil influx. As a consequence, Ifnar1⁻/⁻ mice recruit more neutrophils after influenza infection than do WT mice. Treatment of IFNAR1 blocking antibody on the WT bone marrow (BM) cells in vitro failed to differentiate into Ly6C(hi) monocytes. By using BM chimeric mice (WT BM into Ifnar1⁻/⁻ and vice versa), we confirmed that IFN-I signaling in hematopoietic cells is required for the generation of Ly6C(hi) monocytes. Of note, WT BM reconstituted Ifnar1⁻/⁻ chimeric mice with increased numbers of Ly6C(hi) monocytes survived longer than influenza-infected Ifnar1⁻/⁻ mice. In contrast, WT mice that received Ifnar1⁻/⁻ BM cells with alternative Ly6C(int) monocytes and increased numbers of neutrophils exhibited higher mortality rates than WT mice given WT BM cells. Collectively, these data suggest that IFN-I contributes to resistance of influenza infection by control of monocytes and neutrophils in the lung.
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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.