ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Chlamydia pneumoniae impairs the innate immune response in infected epithelial cells by targeting TRAF3.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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
9 citing papers in PubMed, 16 citations in OpenAlex.
- Review
- C3aR plays both sides in regulating resistance to bacterial infections.PLoS pathogens · 2022Review
- Interferons: Tug of War Between Bacteria and Their Host.Frontiers in cellular and infection microbiology · 2021Review
- Mechanisms of Epithelial Immunity Evasion by Respiratory Bacterial Pathogens.Frontiers in immunology · 2020Review
- Clear Victory forFrontiers in microbiology · 2019Review
- Chlamydia cell biology and pathogenesis.Nature reviews. Microbiology · 2016Review
- Host immune responses after hypoxic reactivation of IFN-γ induced persistent Chlamydia trachomatis infection.Frontiers in cellular and infection microbiology · 2014Article
- Article
- Evidence for horizontal gene transfer betweenBacteriophageArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Type I IFNs are induced during microbial infections and have well-characterized antiviral activities. TRAF3 is a signaling molecule crucial for type I IFN production and, therefore, represents a potential target for disarming immune responses. Chlamydia pneumoniae is a human pathogen that primarily infects respiratory epithelial cells; the onset of symptoms takes several weeks, and the course of infection is protracted. C. pneumoniae has also been associated with a variety of chronic inflammatory conditions. Thus, typical C. pneumoniae infections of humans are consistent with an impairment in inflammatory responses to the microorganism. We demonstrate that infection of epithelial cells with C. pneumoniae does not lead to IFN-β production. Instead, infected cells are prevented from activating IFN regulatory factor 3. This effect is mediated by C. pneumoniae-dependent degradation of TRAF3, which is independent of a functional proteasome. Hence, it is likely that C. pneumoniae expresses a unique protease targeting TRAF3-dependent immune effector mechanisms.
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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.