ArticlemBio2010
Autocrine interferon priming in macrophages but not dendritic cells results in enhanced cytokine and chemokine production after coronavirus infection.
Article in mBio, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 45 citations in OpenAlex.
- Heterologous expression of HCoV-HKU1 ORF 7b by mouse hepatitis virus protects against severe disease during murine infection.PLoS pathogens · 2025Article
- Chemokines as potential biomarkers for predicting the course of COVID-19 - a review of the literature.Frontiers in immunology · 2025Review
- Mouse hepatitis virus JHMV I protein is required for maximal virulence.Journal of virology · 2024Article
- Immune Epitopes of SARS-CoV-2 Spike Protein and Considerations for Universal Vaccine Development.ImmunoHorizons · 2024Review
- Immune Epitopes of SARS-CoV-2 Spike Protein and Considerations for Universal Vaccine Development.bioRxiv : the preprint server for biology · 2023Article
- Review
- Toll-like Receptor Mediation in SARS-CoV-2: A Therapeutic Approach.International journal of molecular sciences · 2022Review
- Infectious Bronchitis Virus Nsp14 Degrades JAK1 to Inhibit the JAK-STAT Signaling Pathway in HD11 Cells.Viruses · 2022Article
- Article
- The N-Terminal Region of Middle East Respiratory Syndrome Coronavirus Accessory Protein 8b Is Essential for Enhanced Virulence of an Attenuated Murine Coronavirus.Journal of virology · 2022Article
- TLR2 senses the SARS-CoV-2 envelope protein to produce inflammatory cytokines.Nature immunology · 2021Article
- SARS-CoV-2 takes its Toll.Nature immunology · 2021Article
- Cellular and Molecular Effects of SARS-CoV-2 Linking Lung Infection to the Brain.Frontiers in immunology · 2021Review
- Impaired NLRP3 inflammasome activation/pyroptosis leads to robust inflammatory cell death via caspase-8/RIPK3 during coronavirus infection.The Journal of biological chemistry · 2020Article
- A dissection of SARS‑CoV2 with clinical implications (Review).International journal of molecular medicine · 2020Review
- Coronavirus Endoribonuclease and Deubiquitinating Interferon Antagonists Differentially Modulate the Host Response during Replication in Macrophages.Journal of virology · 2020Article
- IFN-I response timing relative to virus replication determines MERS coronavirus infection outcomes.The Journal of clinical investigation · 2019Article
- The coronavirus macrodomain is required to prevent PARP-mediated inhibition of virus replication and enhancement of IFN expression.PLoS pathogens · 2019Article
- Virus-induced inflammasome activation is suppressed by prostaglandin DProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Early endonuclease-mediated evasion of RNA sensing ensures efficient coronavirus replication.PLoS pathogens · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Coronaviruses efficiently inhibit interferon (IFN) induction in nonhematopoietic cells and conventional dendritic cells (cDC). However, IFN is produced in infected macrophages, microglia, and plasmacytoid dendritic cells (pDC). To begin to understand why IFN is produced in infected macrophages, we infected bone marrow-derived macrophages (BMM) and as a control, bone marrow-derived DC (BMDC) with the coronavirus mouse hepatitis virus (MHV). As expected, BMM but not BMDC expressed type I IFN. IFN production in infected BMM was nearly completely dependent on signaling through the alpha/beta interferon (IFN-α/β) receptor (IFNAR). Several IFN-dependent cytokines and chemokines showed the same expression pattern, with enhanced production in BMM compared to BMDC and dependence upon signaling through the IFNAR. Exogenous IFN enhanced IFN-dependent gene expression in BMM at early times after infection and in BMDC at all times after infection but did not stimulate expression of molecules that signal through myeloid differentiation factor 88 (MyD88), such as tumor necrosis factor (TNF). Collectively, our results show that IFN is produced at early times postinfection (p.i.) in MHV-infected BMM, but not in BMDC, and primes expression of IFN and IFN-responsive genes. Further, our results also show that BMM are generally more responsive to MHV infection, since MyD88-dependent pathways are also activated to a greater extent in these cells than in BMDC.
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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.