ArticleJournal of immunology (Baltimore, Md. : 1950)2013
CD4+ T cell expression of MyD88 is essential for normal resolution of Chlamydia muridarum genital tract infection.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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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
12 citing papers in PubMed, 19 citations in OpenAlex.
- Diverse animal models forFrontiers in microbiology · 2024Review
- Myeloid MyD88 restricts CD8Scientific reports · 2023Article
- Gut dysbiosis contributes to chlamydial induction of hydrosalpinx in the upper genital tract.Frontiers in microbiology · 2023Article
- Cytotoxic CD4eLife · 2022Article
- T Cell-Independent Gamma Interferon and B Cells Cooperate To Prevent Mortality Associated with Disseminated Chlamydia muridarum Genital Tract Infection.Infection and immunity · 2018Article
- VIPER regulates naive T cell activation and effector responses: Implication in TLR4 associated acute stage T cell responses.Scientific reports · 2018Article
- Article
- T cell expression of IL-18R and DR3 is essential for non-cognate stimulation of Th1 cells and optimal clearance of intracellular bacteria.PLoS pathogens · 2017Article
- Chlamydial Plasmid-Dependent Pathogenicity.Trends in microbiology · 2017Review
- 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
- Plasmid-encoded Pgp3 is a major virulence factor for Chlamydia muridarum to induce hydrosalpinx in mice.Infection and immunity · 2014Article
- Reduced live organism recovery and lack of hydrosalpinx in mice infected with plasmid-free Chlamydia muridarum.Infection and immunity · 2014Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Resolution of Chlamydia genital tract infection is delayed in the absence of MyD88. In these studies, we first used bone marrow chimeras to demonstrate a requirement for MyD88 expression by hematopoietic cells in the presence of a wild-type epithelium. Using mixed bone marrow chimeras we then determined that MyD88 expression was specifically required in the adaptive immune compartment. Furthermore, adoptive transfer experiments revealed that CD4(+) T cell expression of MyD88 was necessary for normal resolution of genital tract infection. This requirement was associated with a reduced ability of MyD88(-/-)CD4(+) T cells to accumulate in the draining lymph nodes and genital tract when exposed to the same inflammatory milieu as wild-type CD4(+) T cells. We also demonstrated that the impaired infection control we observed in the absence of MyD88 could not be recapitulated by deficiencies in TLR or IL-1R signaling. In vitro, we detected an increased frequency of apoptotic MyD88(-/-)CD4(+) T cells upon activation in the absence of exogenous ligands for receptors upstream of MyD88. These data reveal an intrinsic requirement for MyD88 in CD4(+) T cells during Chlamydia infection and indicate that the importance of MyD88 extends beyond innate immune responses by directly influencing adaptive immunity.
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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.