ArticleFEMS immunology and medical microbiology2009
Identification of dendritic cell subsets responding to genital infection by Chlamydia muridarum.
Article in FEMS immunology and medical microbiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Modulation of T helper 1 and T helper 2 immune balance in a murine stress model during Chlamydia muridarum genital infection.PloS one · 2020Article
- IL-10 Producing B Cells Dampen Protective T Cell Response and AllowFrontiers in immunology · 2019Article
- Alternatively Activated Macrophages Are Host Cells forFrontiers in microbiology · 2019Article
- Clear Victory forFrontiers in microbiology · 2019Review
- Expression of CXCR3 on Adaptive and Innate Immune Cells Contributes Oviduct Pathology throughoutJournal of mucosal immunology research · 2017Article
- The role of dendritic cells in driving genital tract inflammation and HIV transmission risk: are there opportunities to intervene?Innate immunity · 2015Review
- Significant roles played by IL-10 in Chlamydia infections.Inflammation · 2014Review
- Article
- The female lower genital tract is a privileged compartment with IL-10 producing dendritic cells and poor Th1 immunity following Chlamydia trachomatis infection.PLoS pathogens · 2010Article
- Plasmacytoid dendritic cells modulate nonprotective T-cell responses to genital infection by Chlamydia muridarum.FEMS immunology and medical microbiology · 2010Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Dendritic cells (DCs) are central for the induction of T-cell responses needed for chlamydial eradication. Here, we report the activation of two DC subsets: a classical CD11b+ (cDC) and plasmacytoid (pDC) during genital infection with Chlamydia muridarum. Genital infection induced an influx of cDC and pDC into the genital tract and its draining lymph node (iliac lymph nodes, ILN) as well as colocalization with T cells in the ILN. Genital infection with C. muridarum also stimulated high levels of costimulatory molecules on cDC central for the activation of naïve T cells in vivo. In contrast, pDC expressed low levels of most costimulatory molecules in vivo and did not secrete cytokines associated with the production of T helper (Th)1 cells in vitro. However, pDC upregulated inducible costimulatory ligand expression and produced IL-6 and IL-10 in response to chlamydial exposure in vitro. Our findings show that these two DC subsets likely have different functions in vivo. cDCs are prepared for induction of antichlamydial T-cell responses, whereas pDCs have characteristics associated with the differentiation of non-Th1 cell subsets.
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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.