ReviewCellular microbiology2010
Induction of type I interferons by bacteria.
Review in Cellular microbiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 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
83 citing papers in PubMed, 142 citations in OpenAlex.
- Human TLR8 is activated upon recognition of Borrelia burgdorferi RNA in the phagosome of human monocytes.Journal of leukocyte biology · 2013Trial
- Noncanonical bactericidal activity of teleost type I interferon is conferred by a membrane-targeting C-terminal peptide.PLoS pathogens · 2026Article
- Characterization of a novel cell wall-associated nucleotidase of Enterococcus faecalis that degrades extracellular c-di-AMP.PLoS pathogens · 2026Article
- Biomarkers for predicting immunotherapy response and resistance in glioblastoma.Frontiers in immunology · 2026Review
- Mycobacterial ESAT-6 triggers cGAS-STING pathway via the GSDMD-NT dependent mitochondria dysfunction.Virulence · 2025Article
- Single-cell atlas of grass carp (Zoological research · 2025Article
- Borrelia burgdorferi c-di-AMP is a key extracellular pathogen-associated molecular pattern to elicit type I interferon responses in mammalian hosts.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Type I interferons in bacterial diseases: myeloid cells at the crossroads of protection and pathology.Frontiers in immunology · 2025Review
- Article
- Cathelicidin CATH-B1 Inhibits Pseudorabies Virus Infection via Direct Interaction and TLR4/JNK/IRF3-Mediated Interferon Activation.Journal of virology · 2023Article
- Review
- Pseudomonas aeruginosa Induces Interferon-β Production to Promote Intracellular Survival.Microbiology spectrum · 2022Article
- Macrophage inflammatory state influences susceptibility to lysosomal damage.Journal of leukocyte biology · 2022Article
- Article
- Article
- Immunological Perspective:Mediators of inflammation · 2022Review
- Extrahepatic factors in hepatic immune regulation.Frontiers in immunology · 2022Review
- Foundational concepts in the biology of bacterial keratitis.Experimental eye research · 2021Review
- SARS-CoV-2 and immune-microbiome interactions: Lessons from respiratory viral infections.International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases · 2021Review
- Article
23 more citing papers are in PubMed but not listed here.
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
Type I interferons (IFNs) are secreted cytokines that orchestrate diverse immune responses to infection. Although typically considered to be most important in the response to viruses, type I IFNs are also induced by most, if not all, bacterial pathogens. Although diverse mechanisms have been described, bacterial induction of type I IFNs occurs upon stimulation of two main pathways: (i) Toll-like receptor (TLR) recognition of bacterial molecules such as lipopolysaccharide (LPS); (ii) TLR-independent recognition of molecules delivered to the host cell cytosol. Cytosolic responses can be activated by two general mechanisms. First, viable bacteria can secrete stimulatory ligands into the cytosol via specialized bacterial secretion systems. Second, ligands can be released from bacteria that lyse or are degraded. The bacterial ligands that induce the cytosolic pathways remain uncertain in many cases, but appear to include various nucleic acids. In this review, we discuss recent advances in our understanding of how bacteria induce type I interferons and the roles type I IFNs play in host immunity.
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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.