ArticleGenes and immunity2006
Genetic analysis of susceptibility to Chlamydia trachomatis in mouse.
Article in Genes and immunity, 2006. 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.
- ThemBio · 2026Article
- Emerging Insights into Protein Post-Translational Modifications in Chlamydia-Host Interactions.The American journal of pathology · 2025Review
- Article
- Human genetic diversity regulating theHGG advances · 2022Article
- Early Colonization of the Upper Genital Tract by Chlamydia muridarum Is Associated with Enhanced Inflammation Later in Infection.Infection and immunity · 2019Article
- Article
- Indoleamine 2,3-Dioxygenase Activity inFrontiers in cellular and infection microbiology · 2019Article
- Influenza Pathogenesis in Genetically Defined Resistant and Susceptible Murine Strains .The Yale journal of biology and medicine · 2017Review
- Comparison of Murine Cervicovaginal Infection by Chlamydial Strains: Identification of Extrusions ShedFrontiers in cellular and infection microbiology · 2017Article
- Article
- Dendritic cell function and pathogen-specific T cell immunity are inhibited in mice administered levonorgestrel prior to intranasal Chlamydia trachomatis infection.Scientific reports · 2016Article
- Sensing the enemy, containing the threat: cell-autonomous immunity to Chlamydia trachomatis.FEMS microbiology reviews · 2016Review
- IRGB10 Liberates Bacterial Ligands for Sensing by the AIM2 and Caspase-11-NLRP3 Inflammasomes.Cell · 2016Article
- Interferon-Inducible GTPases in Host Resistance, Inflammation and Disease.Journal of molecular biology · 2016Review
- Article
- Guanylate binding proteins enable rapid activation of canonical and noncanonical inflammasomes in Chlamydia-infected macrophages.Infection and immunity · 2015Article
- An Excess of the Proinflammatory Cytokines IFN-γ and IL-12 Impairs the Development of the Memory CD8+ T Cell Response to Chlamydia trachomatis.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- VACCINES. A mucosal vaccine against Chlamydia trachomatis generates two waves of protective memory T cells.Science (New York, N.Y.) · 2015Article
- Article
- Genetic variation in Chlamydia trachomatis and their hosts: impact on disease severity and tissue tropism.Future microbiology · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Chlamydia trachomatis is a bacterial pathogen that is a major cause of blindness and infertility in diverse populations across the world. In an effort to model genetic complexities that are observed in human populations and to identify novel genes involved in susceptibility to C. trachomatis, we have adapted a murine model of systemic infection for use in genetic analysis. In this model, chlamydial colonization and replication is measured in the spleens of mice shortly after intravenous delivery of C. trachomatis L2. Here, we show that C57BL/6J and C3H/HeJ inbred mice are differentially susceptible to this systemic infection. Additionally, fibroblasts cultured from C57BL/6J and C3H/HeJ embryos are differentially permissive for chlamydial replication. We have taken advantage of this natural variation to map quantitative trait loci on Chromosomes 2, 3, and 11 that segregate with the bacterial load in F2 cross progeny during the acute phase of C. trachomatis infection in vivo. To validate our mapping results, we also generated mice that are congenic for a portion of Chromosome 11 from the susceptible parent. This congenic interval confers increased susceptibility to C. trachomatis, both in vivo and in vitro, suggesting that our screen identified at least one gene that is involved in cellular resistance to C. trachomatis replication.
Indexed as
Identifiers
16395389What 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.