ArticlePLoS pathogens2010
The female lower genital tract is a privileged compartment with IL-10 producing dendritic cells and poor Th1 immunity following Chlamydia trachomatis infection.
Article in PLoS pathogens, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 64 citations in OpenAlex.
- Chlamydia trachomatis orchestrates multifaceted host cell manipulation for immune evasion.Communications biology · 2026Review
- The emerging role of effector functions exerted by tissue-resident memory T cells.Oxford open immunology · 2024Review
- Longitudinal changes in tear cytokines and antimicrobial proteins in trachomatous disease.PLoS neglected tropical diseases · 2023Article
- Interleukin-27 (IL-27) Promotes Chlamydial Infection in the Female Genital Tract.Infection and immunity · 2022Article
- Repeat infections with chlamydia in women may be more transcriptionally active with lower responses from some immune genes.Frontiers in public health · 2022Article
- Modulation of T helper 1 and T helper 2 immune balance in a murine stress model during Chlamydia muridarum genital infection.PloS one · 2020Article
- High expression of IDO1 and TGF-β1 during recurrence and post infection clearance with Chlamydia trachomatis, are independent of host IFN-γ response.BMC infectious diseases · 2019Article
- Alternatively Activated Macrophages Are Host Cells forFrontiers in microbiology · 2019Article
- IL-10 Producing B Cells Dampen Protective T Cell Response and AllowFrontiers in immunology · 2019Article
- Toll-like receptor 3 (TLR3) promotes the resolution of Chlamydia muridarum genital tract infection in congenic C57BL/6N mice.PloS one · 2018Article
- IL-4-secreting eosinophils promote endometrial stromal cell proliferation and preventProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Chlamydia trachomatis Cellular Exit Alters Interactions with Host Dendritic Cells.Infection and immunity · 2017Article
- Dampened antiviral immunity to intravaginal exposure to RNA viral pathogens allows enhanced viral replication.The Journal of experimental medicine · 2016Article
- Article
- Interleukin-10 modulates antigen presentation by dendritic cells through regulation of NLRP3 inflammasome assembly during Chlamydia infection.Infection and immunity · 2015Article
- Chlamydia muridarum infection associated host MicroRNAs in the murine genital tract and contribution to generation of host immune response.American journal of reproductive immunology (New York, N.Y. : 1989) · 2015Article
- NOD1 in contrast to NOD2 functional polymorphism influence Chlamydia trachomatis infection and the risk of tubal factor infertility.Pathogens and disease · 2015Article
- CD43-, but not CD43+, IL-10-producing CD1dhiCD5+ B cells suppress type 1 immune responses during Chlamydia muridarum genital tract infection.Mucosal immunology · 2015Article
- Increased susceptibility to vaginal simian/human immunodeficiency virus transmission in pig-tailed macaques coinfected with Chlamydia trachomatis and Trichomonas vaginalis.The Journal of infectious diseases · 2014Article
- In vivo whole animal body imaging reveals colonization of Chlamydia muridarum to the lower genital tract at early stages of infection.Molecular imaging and biology · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
While a primary genital tract infection with C. trachomatis stimulates partial-protection against re-infection, it may also result in severe inflammation and tissue destruction. Here we have dissected whether functional compartments exist in the genital tract that restrict Th1-mediated protective immunity. Apart from the Th1-subset, little is known about the role of other CD4(+) T cell subsets in response to a genital tract chlamydial infection. Therefore, we investigated CD4(+) T cell subset differentiation in the genital tract using RT-PCR for expression of critical transcription factors and cytokines in the upper (UGT) and lower genital tract (LGT) of female C57BL/6 mice in response to C. trachomatis serovar D infection. We found that the Th1 subset dominated the UGT, as IFN-γ and T-bet mRNA expression were high, while GATA-3 was low following genital infection with C. trachomatis serovar D. By contrast, IL-10 and GATA-3 mRNA dominated the LGT, suggesting the presence of Th2 cells. These functional compartments also attracted regulatory T cells (Tregs) differently as increased FoxP3 mRNA expression was seen primarily in the UGT. Although IL-17A mRNA was somewhat up-regulated in the LGT, no significant change in RORγ-t mRNA expression was observed, suggesting no involvement of Th17 cells. The dichotomy between the LGT and UGT was maintained during infection by IL-10 because in IL-10-deficient mice the distinction between the two compartments was completely lost and a dramatic shift to the predominance of Th1 cells in the LGT occurred. Unexpectedly, the major source of IL-10 was CD11c(+) CD11b(+) DC, probably creating an anti-inflammatory privileged site in the LGT.
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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.