ArticleJournal of immunology (Baltimore, Md. : 1950)2011
IFN-β mediates suppression of IL-12p40 in human dendritic cells following infection with virulent Francisella tularensis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 41 citations in OpenAlex.
- CLEC-1 promotes early IFN response in cDC1s and favors immune dysregulation during sepsis in mice.iScience · 2026Article
- Type I interferon signaling promotes early innate control ofbioRxiv : the preprint server for biology · 2026Article
- Glutamate utilization fuels rapid production of mitochondrial ROS in dendritic cells and drives systemic inflammation during tularemia.Science advances · 2025Article
- The dual role of type I interferons in bacterial infections: from immune defense to pathogenesis.mBio · 2025Review
- The immune response toFrontiers in microbiology · 2025Review
- Type I interferons in bacterial diseases: myeloid cells at the crossroads of protection and pathology.Frontiers in immunology · 2025Review
- Autophagy and Bacterial infections.Autophagy reports · 2025Review
- Pathogenicity and virulence ofVirulence · 2023Review
- Macrophages Demonstrate Guanylate-Binding Protein-Dependent and Bacterial Strain-Dependent Responses toFrontiers in cellular and infection microbiology · 2021Article
- NLRP3 inflammasome pathway has a critical role in the host immunity against clinically relevant Acinetobacter baumannii pulmonary infection.Mucosal immunology · 2018Article
- The Early Dendritic Cell Signaling Induced by VirulentMolecular & cellular proteomics : MCP · 2018Article
- Hematopoietic MyD88 and IL-18 are essential for IFN-γ-dependent restriction of type AJournal of leukocyte biology · 2017Article
- Metabolic Reprogramming of Host Cells by Virulent Francisella tularensis for Optimal Replication and Modulation of Inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Early Interactions of Murine Macrophages with Francisella tularensis Map to Mouse Chromosome 19.mBio · 2016Article
- Virulent Francisella tularensis destabilize host mRNA to rapidly suppress inflammation.Journal of innate immunity · 2014Article
- Virulent Type A Francisella tularensis actively suppresses cytokine responses in human monocytes.Frontiers in cellular and infection microbiology · 2014Article
- Mitochondrial ROS potentiates indirect activation of the AIM2 inflammasome.Frontiers in microbiology · 2014Article
- Bacterial programming of host responses: coordination between type I interferon and cell death.Frontiers in microbiology · 2014Review
- Immunotherapy for tularemia.Virulence · 2013Review
- Lipids derived from virulent Francisella tularensis broadly inhibit pulmonary inflammation via toll-like receptor 2 and peroxisome proliferator-activated receptor α.Clinical and vaccine immunology : CVI · 2013Article
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 2 institutions in 1 country.
Funding
Abstract
Active suppression of inflammation is a strategy used by many viral and bacterial pathogens, including virulent strains of the bacterium Francisella tularensis, to enable colonization and infection in susceptible hosts. In this study, we demonstrated that virulent F. tularensis strain SchuS4 selectively inhibits production of IL-12p40 in primary human cells via induction of IFN-β. In contrast to the attenuated live vaccine strain, infection of human dendritic cells with virulent SchuS4 failed to induce production of many cytokines associated with inflammation (e.g., TNF-α and IL-12p40). Furthermore, SchuS4 actively suppressed secretion of these cytokines. Assessment of changes in the expression of host genes associated with suppression of inflammatory responses revealed that SchuS4, but not live vaccine strain, induced IFN-β following infection of human dendritic cells. Phagocytosis of SchuS4 and endosomal acidification were required for induction of IFN-β. Further, using a defined mutant of SchuS4, we demonstrated that the presence of bacteria in the cytosol was required, but not sufficient, for induction of IFN-β. Surprisingly, unlike previous reports, induction of IFN-β by F. tularensis was not required for activation of the inflammasome, was not associated with exacerbation of inflammatory responses, and did not control SchuS4 replication when added exogenously. Rather, IFN-β selectively suppressed the ability of SchuS4-infected dendritic cells to produce IL-12p40. Together, these data demonstrated a novel mechanism by which virulent bacteria, in contrast to attenuated strains, modulate human cells to cause disease.
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.