ArticleInfection and immunity2023
Type-I Interferon Signaling Protects against Chlamydia trachomatis Infection in the Female Lower Genital Tract.
Article in Infection and immunity, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Quantifying Chlamydia in the Mouse Gastrointestinal Tract.Methods in molecular biology (Clifton, N.J.) · 2027Article
- The ubiquitin ligase CBL and Fas-associated factor 2 cooperate to regulate the innate immune response to M. tuberculosis.PLoS pathogens · 2026Article
- Single-cell atlas of cervical organoids uncovers epithelial immune heterogeneity and intercellular cross-talk during Chlamydia infection.Science advances · 2025Article
- The dual role of type I interferons in bacterial infections: from immune defense to pathogenesis.mBio · 2025Review
- The balance between antiviral and antibacterial responses duringbioRxiv : the preprint server for biology · 2024Article
- Regulation of chlamydial spreading from the small intestine to the large intestine by IL-22-producing CD4Infection and immunity · 2024Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
We have previously shown that Chlamydia trachomatis is significantly inhibited during the early stage of infection in the female mouse lower genital tract and the anti-C. trachomatis innate immunity is compromised in the absence of cGAS-STING signaling. Since type-I interferon is a major downstream response of the cGAS-STING signaling, we evaluated the effect of type-I interferon signaling on C. trachomatis infection in the female genital tract in the current study. The infectious yields of chlamydial organisms recovered from vaginal swabs along the infection course were carefully compared between mice with or without deficiency in type-I interferon receptor (IFNαR1) following intravaginal inoculation with 3 different doses of C. trachomatis. It was found that IFNαR1-deficient mice significantly increased the yields of live chlamydial organisms on days 3 and 5, providing the 1st experimental evidence for a protective role of type-I interferon signaling in preventing C. trachomatis infection in mouse female genital tract. Further comparison of live C. trachomatis recovered from different genital tract tissues between wild type and IFNαR1-deficient mice revealed that the type-I interferon-dependent anti-C. trachomatis immunity was restricted to mouse lower genital tract. This conclusion was validated when C. trachomatis was inoculated transcervically. Thus, we have demonstrated an essential role of type-I interferon signaling in innate immunity against C. trachomatis infection in the mouse lower genital tract, providing a platform for further revealing the molecular and cellular basis of type-I interferon-mediated immunity against sexually transmitted infection with C. trachomatis.
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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.