ArticleBMC infectious diseases2011
Enhanced upper genital tract pathologies by blocking Tim-3 and PD-L1 signaling pathways in mice intravaginally infected with Chlamydia muridarum.
Article in BMC infectious diseases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- STING agonists reduce genital chlamydial infection and attenuate inflammation and pathology.Infection and immunity · 2026Article
- Walking the tightrope: Balancing immune checkpoints and their inhibitors in host defence against bacterial infections.Journal of applied biomedicine · 2026Review
- Invariant and Diverse NKT Cells Regulate Bacterial Clearance and Pathology in Chlamydial Genital Tract Infection in Mice.Pathogens (Basel, Switzerland) · 2025Article
- Type I IFNs contribute to upregulation of PD-L1 duringInfection and immunity · 2025Article
- Article
- Gut dysbiosis contributes to chlamydial induction of hydrosalpinx in the upper genital tract.Frontiers in microbiology · 2023Article
- Preparation of graphene oxide-stabilized Pickering emulsion adjuvant for Pgp3 recombinant vaccine and enhanced immunoprotection againstFrontiers in immunology · 2023Article
- The PD-1/PD-L1 pathway is induced during Borrelia burgdorferi infection and inhibits T cell joint infiltration without compromising bacterial clearance.PLoS pathogens · 2022Article
- Efficacy of Pgp3 vaccination forFrontiers in immunology · 2022Article
- T cell responses to Chlamydia.Pathogens and disease · 2021Review
- Infection-driven activation of transglutaminase 2 boosts glucose uptake and hexosamine biosynthesis in epithelial cells.The EMBO journal · 2020Article
- Review
- Modeling the transcriptome of genital tract epithelial cells and macrophages in healthy mucosa versus mucosa inflamed by Chlamydia muridarum infection.Pathogens and disease · 2015Article
- Intrauterine infection with plasmid-free Chlamydia muridarum reveals a critical role of the plasmid in chlamydial ascension and establishes a model for evaluating plasmid-independent pathogenicity.Infection and immunity · 2015Article
- Chlamydia muridarum induction of glandular duct dilation in mice.Infection and immunity · 2015Article
- In vitro passage selects for Chlamydia muridarum with enhanced infectivity in cultured cells but attenuated pathogenicity in mouse upper genital tract.Infection and immunity · 2015Article
- Plasmid-Encoded Pgp5 Is a Significant Contributor to Chlamydia muridarum Induction of Hydrosalpinx.PloS one · 2015Article
- Neisseria gonorrhoeae Modulates Immunity by Polarizing Human Macrophages to a M2 Profile.PloS one · 2015Article
- Plasmid-encoded Pgp3 is a major virulence factor for Chlamydia muridarum to induce hydrosalpinx in mice.Infection and immunity · 2014Article
- PD-L1 limits the mucosal CD8+ T cell response to Chlamydia trachomatis.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlthough Tim-3 & PD-L1 signaling pathways play important roles in negatively regulating immune responses, their roles in chlamydial infection have not been evaluated.
methodsNeutralization antibodies targeting Tim-3 and PD-L1 were used to treat mice. Following an intravaginal infection with C. muridarum organisms, mice with or without the dual antibody treatment were compared for live chlamydial organism shedding from the lower genital tract and inflammatory pathology in the upper genital tract.
resultsMice treated with anti-Tim-3 and anti-PD-L1 antibodies displayed a time course of live organism shedding similar to that of mice treated with equivalent amounts of isotype-matched IgG molecules. The combined antibody blocking failed to alter either the lower genital tract cytokine or systemic humoral and cellular adaptive responses to C. muridarum infection. However, the antibody blocking significantly enhanced C. muridarum-induced pathologies in the upper genital tract, including more significant hydrosalpinx and inflammatory infiltration in uterine horn and oviduct tissues.
conclusionsThe Tim-3 and PD-L1-mediated signaling can significantly reduce pathologies in the upper genital tract without suppressing immunity against chlamydial infection, suggesting that Tim-3 and PD-L1-mediated negative regulation may be manipulated to attenuate tubal pathologies in women persistently infected with C. trachomatis organisms.
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