ArticleFrontiers in cellular and infection microbiology2016
Coxiella burnetii Induces Inflammatory Interferon-Like Signature in Plasmacytoid Dendritic Cells: A New Feature of Immune Response in Q Fever.
Article in Frontiers in cellular and infection microbiology, 2016. 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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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- Review
- Q Fever Vaccines: Unveiling the Historical Journey and Contemporary Innovations in Vaccine Development.Vaccines · 2025Review
- Cytometry profiling ofFrontiers in immunology · 2023Article
- Recent Advances on the Innate Immune Response toFrontiers in cellular and infection microbiology · 2021Review
- T-Bet Controls Susceptibility of Mice toFrontiers in microbiology · 2020Article
- Article
- RETRACTED: A transcriptional signature associated with non-Hodgkin lymphoma in the blood of patients with Q fever.PloS one · 2019Article
- Emerging Roles of Autophagy and Inflammasome in Ehrlichiosis.Frontiers in immunology · 2019Review
- High Concentrations of Serum Soluble E-Cadherin in Patients With Q Fever.Frontiers in cellular and infection microbiology · 2019Article
- Full-Term Human Placental Macrophages EliminateFrontiers in microbiology · 2019Article
- Viable Coxiella burnetii Induces Differential Cytokine Responses in Chronic Q Fever Patients Compared to Heat-Killed Coxiella burnetii.Infection and immunity · 2018Article
- Getting "Inside" Type I IFNs: Type I IFNs in Intracellular Bacterial Infections.Journal of immunology research · 2017Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Plasmacytoid dendritic cells (pDCs) play a major role in antiviral immunity via the production of type I interferons (IFNs). There is some evidence that pDCs interact with bacteria but it is not yet clear whether they are protective or contribute to bacterial pathogenicity. We wished to investigate whether Coxiella burnetii, the agent of Q fever, interacts with pDCs. The stimulation of pDCs with C. burnetii increased the expression of activation and migratory markers (CD86 and CCR7) as determined by flow cytometry and modulated gene expression program as revealed by a microarray approach. Indeed, genes encoding for pro-inflammatory cytokines, chemokines, and type I INF were up-regulated. The up-regulation of type I IFN was correlated with an increase in IFN-α release by C. burnetii-stimulated pDCs. We also investigated pDCs in patients with Q fever endocarditis. Using flow cytometry and a specific gating strategy, we found that the number of circulating pDCs was significantly lower in patients with Q fever endocarditis as compared to healthy donors. In addition, the remaining circulating pDCs expressed activation and migratory markers. As a whole, our study identified non-previously reported activation of pDCs by C. burnetii and their modulation during Q fever.
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