ArticleInfection and immunity1999
Clearance of Chlamydia trachomatis from the murine genital mucosa does not require perforin-mediated cytolysis or Fas-mediated apoptosis.
Article in Infection and immunity, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 60 citations in OpenAlex.
- T cell responses to Chlamydia.Pathogens and disease · 2021Review
- Immunopathogenesis of genital Chlamydia infection: insights from mouse models.Pathogens and disease · 2021Review
- A Class II-Restricted CD8γ13 T-Cell Clone Protects During Chlamydia muridarum Genital Tract Infection.The Journal of infectious diseases · 2020Article
- An Ancient Molecular Arms Race:Frontiers in immunology · 2020Review
- CD8+ T cells define an unexpected role in live-attenuated vaccine protective immunity against Chlamydia trachomatis infection in macaques.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Vaginal chlamydial clearance following primary or secondary infection in mice occurs independently of TNF-α.Frontiers in cellular and infection microbiology · 2013Article
- Perforin is detrimental to controlling [corrected] C. muridarum replication in vitro, but not in vivo.PloS one · 2013Article
- The major CD8 T cell effector memory subset in the normal and Chlamydia trachomatis-infected human endocervix is low in perforin.BMC immunology · 2012Article
- Plac8-dependent and inducible NO synthase-dependent mechanisms clear Chlamydia muridarum infections from the genital tract.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Article
- Enhanced upper genital tract pathologies by blocking Tim-3 and PD-L1 signaling pathways in mice intravaginally infected with Chlamydia muridarum.BMC infectious diseases · 2011Article
- Tumor necrosis factor alpha production from CD8+ T cells mediates oviduct pathological sequelae following primary genital Chlamydia muridarum infection.Infection and immunity · 2011Article
- Chlamydia-specific CD4 T cell clones control Chlamydia muridarum replication in epithelial cells by nitric oxide-dependent and -independent mechanisms.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Article
- Human guanylate binding proteins potentiate the anti-chlamydia effects of interferon-gamma.PloS one · 2009Article
- A MyD88-dependent early IL-17 production protects mice against airway infection with the obligate intracellular pathogen Chlamydia muridarum.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- Article
- Novel Chlamydia muridarum T cell antigens induce protective immunity against lung and genital tract infection in murine models.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- The chlamydial plasmid-encoded protein pgp3 is secreted into the cytosol of Chlamydia-infected cells.Infection and immunity · 2008Article
- Caspase-1 contributes to Chlamydia trachomatis-induced upper urogenital tract inflammatory pathologies without affecting the course of infection.Infection and immunity · 2008Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The molecular mechanisms of resistance to genital infection with the mouse pneumonitis (MoPn) strain of Chlamydia trachomatis are unknown. A role for major histocompatibility complex class II-restricted, interleukin-12-dependent CD4(+) T cells has been established, but the functional activity of these cells does not depend on secretion of gamma interferon. Here we examined the potential contribution of T-cell-mediated cytotoxicity and apoptosis to mucosal clearance of MoPn by using mice deficient in the molecular mediators of target cell lysis. Animals lacking perforin, Fas, Fas ligand, or both perforin and Fas ligand were infected genitally with C. trachomatis MoPn and monitored for expression of immunity to chlamydial antigens and clearance of MoPn from the genital mucosa. In each case, the profile of spleen cytokine production, the magnitude of the host antibody response, and the kinetics of chlamydial clearance were similar to those of genetically intact controls. Compensatory overproduction of tumor necrosis factor alpha, an alternate mediator of apoptosis in certain cell types, did not appear to account for the ability of mutant mice to resolve Chlamydia infections. These results fail to support CD4(+) T-cell-mediated apoptosis or CD8(+) T-cell-mediated cytotoxicity as being critical to the clearance of C. trachomatis MoPn urogenital infections.
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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.