ArticleInfection and immunity2011
MyD88 deficiency leads to decreased NK cell gamma interferon production and T cell recruitment during Chlamydia muridarum genital tract infection, but a predominant Th1 response and enhanced monocytic inflammation are associated with infection resolution.
Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 53 citations in OpenAlex.
- Induction and activation of human Th17 by targeting antigens to dendritic cells via dectin-1.Journal of immunology (Baltimore, Md. : 1950) · 2014Trial
- Interferon-β Coordinates Epithelial Immune Networks and Fibrotic Responses DuringbioRxiv : the preprint server for biology · 2026Article
- Lignin/alginate biomaterials as a promising complementary approach in ocular chlamydial infection.Frontiers in cellular and infection microbiology · 2026Article
- Role of IFN-γ from Different Immune Cells inMicroorganisms · 2025Review
- Endoplasmic reticulum: the target of chlamydial manipulation.Archives of microbiology · 2025Review
- Proinflammatory Cytokines in Women with PCOS in Atypical Pathogen Infections.Diagnostics (Basel, Switzerland) · 2025Article
- The Reaction of Innate Lymphoid Cells in the Mouse Female Genital Tract to Chlamydial Infection.Infection and immunity · 2021Article
- Host Genetic Risk Factors for Chlamydia trachomatis-Related Infertility in Women.The Journal of infectious diseases · 2021Article
- Immunopathogenesis of genital Chlamydia infection: insights from mouse models.Pathogens and disease · 2021Review
- Expression of Nutrient Transporters on NK Cells During Murine Cytomegalovirus Infection Is MyD88-Dependent.Frontiers in immunology · 2021Article
- Insights Into Host Cell Cytokines inFrontiers in immunology · 2021Review
- Genital Chlamydia infection in hyperlipidemic mouse models exacerbates atherosclerosis.Atherosclerosis · 2019Article
- Article
- MicroRNA-1 Negatively Regulates Peripheral NK Cell Function via Tumor Necrosis Factor-Like Weak Inducer of Apoptosis (TWEAK) Signaling Pathways During PPRV Infection.Frontiers in immunology · 2019Article
- Polymorphism detection of promoter region of IFN-γ and IL-2 genes and their association with productive traits in Mazandaran native breeder fowls.Journal of genetics · 2018Article
- Toll-like receptor 3 (TLR3) promotes the resolution of Chlamydia muridarum genital tract infection in congenic C57BL/6N mice.PloS one · 2018Article
- AJournal of immunology (Baltimore, Md. : 1950) · 2017Article
- Inflammatory monocytes require type I interferon receptor signaling to activate NK cells via IL-18 during a mucosal viral infection.The Journal of experimental medicine · 2017Article
- A Protective Vaccine against Chlamydia Genital Infection Using Vault Nanoparticles without an Added Adjuvant.Vaccines · 2017Article
- Expression of CXCR3 on Adaptive and Innate Immune Cells Contributes Oviduct Pathology throughoutJournal of mucosal immunology research · 2017Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
We have previously shown that MyD88 knockout (KO) mice exhibit delayed clearance of Chlamydia muridarum genital infection compared to wild-type (WT) mice. A blunted Th1 response and ineffective suppression of the Th2 response were also observed in MyD88 KO mice. The goal of the present study was to investigate specific mechanisms whereby absence of MyD88 leads to these effects and address the compensatory mechanisms in the genital tract that ultimately clear infection in the absence of MyD88. It was observed that NK cells recruited to the genital tract in MyD88 KO mice failed to produce gamma interferon (IFN-γ) mRNA and protein. This defect was associated with decreased local production of interleukin-17 (IL-17), IL-18, and tumor necrosis factor alpha (TNF-α) but normal levels of IL-12p70. Additionally, recruitment of CD4 T cells to the genital tract was reduced in MyD88 KO mice compared to that in WT mice. Although chronic infection in MyD88 KO mice resulted in oviduct pathology comparable to that of WT mice, increased histiocytic inflammation was observed in the uterine horns. This was associated with increased CCL2 levels and recruitment of macrophages as a potential compensatory mechanism. Further deletion of TLR4-TRIF signaling in MyD88 KO mice, using TLR4/MyD88 double-KO mice, did not further compromise host defense against chlamydiae, suggesting that compensatory mechanisms are Toll-like receptor (TLR) independent. Despite some polarization toward a Th2 response, a Th1 response remained predominant in the absence of MyD88, and it provided equivalent protection against a secondary infection as observed in WT 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.