ArticlePLoS pathogens2011
Compensatory T cell responses in IRG-deficient mice prevent sustained Chlamydia trachomatis infections.
Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 49 citations in OpenAlex.
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- BHLHE40 drives protective polyfunctional CD4 T cell differentiation in the female reproductive tract against Chlamydia.PLoS pathogens · 2024Article
- BHLHE40 drives protective polyfunctional CD4 T cell differentiation in the female reproductive tract againstbioRxiv : the preprint server for biology · 2023Article
- Regulation of chlamydial colonization by IFNγ delivered via distinct cells.Trends in microbiology · 2023Review
- Differential Requirement for IRGM Proteins during Tuberculosis Infection in Mice.Infection and immunity · 2023Article
- The bacterial effector GarD shields Chlamydia trachomatis inclusions from RNF213-mediated ubiquitylation and destruction.Cell host & microbe · 2022Article
- How did we get here? Insights into mechanisms of immunity-related GTPase targeting to intracellular pathogens.Current opinion in microbiology · 2022Review
- Immunity-related GTPase IRGM at the intersection of autophagy, inflammation, and tumorigenesis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Review
- Immunopathogenesis of genital Chlamydia infection: insights from mouse models.Pathogens and disease · 2021Review
- T cell responses to Chlamydia.Pathogens and disease · 2021Review
- Innate IFN-γ Is Essential for Systemic Chlamydia muridarum Control in Mice, While CD4 T Cell-Dependent IFN-γ Production Is Highly Redundant in the Female Reproductive Tract.Infection and immunity · 2021Article
- Dynamin-related Irgm proteins modulate LPS-induced caspase-11 activation and septic shock.EMBO reports · 2020Article
- A Nonsurgical Embryo Transfer Technique for Fresh and Cultured Blastocysts in Rats.Journal of the American Association for Laboratory Animal Science : JAALAS · 2020Article
- Article
- Antigen-specific memory and naïve CD4+ T cells following secondary Chlamydia trachomatis infection.PloS one · 2020Article
- The ROP16III-dependent early immune response determines the subacute CNS immune response and type III Toxoplasma gondii survival.PLoS pathogens · 2019Article
- Early Colonization of the Upper Genital Tract by Chlamydia muridarum Is Associated with Enhanced Inflammation Later in Infection.Infection and immunity · 2019Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The obligate intracellular pathogen Chlamydia trachomatis is the most common cause of bacterial sexually transmitted diseases in the United States. In women C. trachomatis can establish persistent genital infections that lead to pelvic inflammatory disease and sterility. In contrast to natural infections in humans, experimentally induced infections with C. trachomatis in mice are rapidly cleared. The cytokine interferon-γ (IFNγ) plays a critical role in the clearance of C. trachomatis infections in mice. Because IFNγ induces an antimicrobial defense system in mice but not in humans that is composed of a large family of Immunity Related GTPases (IRGs), we questioned whether mice deficient in IRG immunity would develop persistent infections with C. trachomatis as observed in human patients. We found that IRG-deficient Irgm1/m3((-/-)) mice transiently develop high bacterial burden post intrauterine infection, but subsequently clear the infection more efficiently than wildtype mice. We show that the delayed but highly effective clearance of intrauterine C. trachomatis infections in Irgm1/m3((-/-)) mice is dependent on an exacerbated CD4(+) T cell response. These findings indicate that the absence of the predominant murine innate effector mechanism restricting C. trachomatis growth inside epithelial cells results in a compensatory adaptive immune response, which is at least in part driven by CD4(+) T cells and prevents the establishment of a persistent infection in mice.
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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.