ArticlePloS one2014
RETRACTED: Imbalance of circulating monocyte subsets and PD-1 dysregulation in Q fever endocarditis: the role of IL-10 in PD-1 modulation.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 19 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- Walking the tightrope: Balancing immune checkpoints and their inhibitors in host defence against bacterial infections.Journal of applied biomedicine · 2026Review
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- Cytometry profiling ofFrontiers in immunology · 2023Article
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- Natural genetic variation in Drosophila melanogaster reveals genes associated with Coxiella burnetii infection.Genetics · 2021Article
- Detection of Immune Checkpoint Receptors - A Current Challenge in Clinical Flow Cytometry.Frontiers in immunology · 2021Review
- Mechanisms of hyperprogressive disease after immune checkpoint inhibitor therapy: what we (don't) know.Journal of experimental & clinical cancer research : CR · 2020Review
- The role of extracellular vesicles and PD-L1 in glioblastoma-mediated immunosuppressive monocyte induction.Neuro-oncology · 2020Article
- High Concentrations of Serum Soluble E-Cadherin in Patients With Q Fever.Frontiers in cellular and infection microbiology · 2019Article
- T-Cell Receptor Diversity and the Control of T-Cell Homeostasis Mark Ebola Virus Disease Survival in Humans.The Journal of infectious diseases · 2018Article
- Viable Coxiella burnetii Induces Differential Cytokine Responses in Chronic Q Fever Patients Compared to Heat-Killed Coxiella burnetii.Infection and immunity · 2018Article
- Coxiella burnetii Lipopolysaccharide: What Do We Know?International journal of molecular sciences · 2017Review
- From Q Fever to Coxiella burnetii Infection: a Paradigm Change.Clinical microbiology reviews · 2017Review
- Coxiella burnetii Induces Inflammatory Interferon-Like Signature in Plasmacytoid Dendritic Cells: A New Feature of Immune Response in Q Fever.Frontiers in cellular and infection microbiology · 2016Article
- Ly6C- Monocytes Regulate Parasite-Induced Liver Inflammation by Inducing the Differentiation of Pathogenic Ly6C+ Monocytes into Macrophages.PLoS pathogens · 2015Article
- Notch Signaling Pathway Was Involved in Regulating Programmed Cell Death 1 Expression during Sepsis-Induced Immunosuppression.Mediators of inflammation · 2015Article
- Article
Corrections and comments
- Retraction · 2026-05-04Concerns/Issues about Human Subject Welfare · Concerns/Issues about Methods · Investigation by Company/Institution · Investigation by Journal/Publisher · Lack of IRB/IACUC Approval and/or Compliance · Upgrade/Update of Prior Notice(s) ·
- Expression of concern · 2022-12-13Investigation by Journal/Publisher · Updated to Retraction ·
- Expression of concern
- Retracted
Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Q fever endocarditis, a severe complication of Q fever, is associated with a defective immune response, the mechanisms of which are poorly understood. We hypothesized that Q fever immune deficiency is related to altered distribution and activation of circulating monocyte subsets. Monocyte subsets were analyzed by flow cytometry in peripheral blood mononuclear cells from patients with Q fever endocarditis and controls. The proportion of classical monocytes (CD14(+)CD16(-) monocytes) was similar in patients and controls. In contrast, the patients with Q fever endocarditis exhibited a decrease in the non-classical and intermediate subsets of monocytes (CD16(+) monocytes). The altered distribution of monocyte subsets in Q fever endocarditis was associated with changes in their activation profile. Indeed, the expression of HLA-DR, a canonical activation molecule, and PD-1, a co-inhibitory molecule, was increased in intermediate monocytes. This profile was not restricted to CD16(+) monocytes because CD4(+) T cells also overexpressed PD-1. The mechanism leading to the overexpression of PD-1 did not require the LPS from C. burnetii but involved interleukin-10, an immunosuppressive cytokine. Indeed, the incubation of control monocytes with interleukin-10 led to a higher expression of PD-1 and neutralizing interleukin-10 prevented C. burnetii-stimulated PD-1 expression. Taken together, these results show that the immune suppression of Q fever endocarditis involves a cross-talk between monocytes and CD4(+) T cells expressing PD-1. The expression of PD-1 may be useful to assess chronic immune alterations in Q fever endocarditis.
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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.