ArticlePLoS pathogens2014
Late engagement of CD86 after influenza virus clearance promotes recovery in a FoxP3+ regulatory T cell dependent manner.
Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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.
The trial behind it
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
35 citing papers in PubMed, 56 citations in OpenAlex.
- T Regulatory Mechanisms in Airway and Interstitial Lung Disease.Seminars in respiratory and critical care medicine · 2025Review
- A Review on Role of Inflammation in Coronavirus Disease.Endocrine, metabolic & immune disorders drug targets · 2024Review
- Regulatory T cell-derived IL-1Ra suppresses the innate response to respiratory viral infection.Nature immunology · 2023Article
- Extracellular vesicles derived from mesenchymal stem cells - a novel therapeutic tool in infectious diseases.Inflammation and regeneration · 2023Review
- Identification of Aedes aegypti salivary gland proteins interacting with human immune receptor proteins.PLoS neglected tropical diseases · 2022Article
- Generation of resolving memory neutrophils through pharmacological training with 4-PBA or genetic deletion of TRAM.Cell death & disease · 2022Article
- Pathogenesis of Respiratory Viral and Fungal Coinfections.Clinical microbiology reviews · 2022Review
- Type 1 regulatory T cell-mediated tolerance in health and disease.Frontiers in immunology · 2022Review
- Erratum: Type 1 regulatory T cell-mediated tolerance in health and disease.Frontiers in immunology · 2022Article
- PD-1 and ICOS counter-regulate tissue resident regulatory T cell development and IL-10 production during flu.Frontiers in immunology · 2022Article
- Effect of Age on Innate and Adaptive Immunity in Hospitalized COVID-19 Patients.Journal of clinical medicine · 2021Article
- Local memory CD4 T cell niches in respiratory viral infection.The Journal of experimental medicine · 2021Article
- Leukocyte trafficking to the lungs and beyond: lessons from influenza for COVID-19.Nature reviews. Immunology · 2021Review
- Review
- Implications of Sex Differences in Immunity for SARS-CoV-2 Pathogenesis and Design of Therapeutic Interventions.Immunity · 2020Review
- Dynamic Natural Killer Cell and T Cell Responses to Influenza Infection.Frontiers in cellular and infection microbiology · 2020Review
- The alarmins IL-1 and IL-33 differentially regulate the functional specialisation of Foxp3Mucosal immunology · 2019Article
- Article
- Article
- Mechanisms of Bacterial Superinfection Post-influenza: A Role for Unconventional T Cells.Frontiers in immunology · 2019Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Influenza A virus (IAV) infection in the respiratory tract triggers robust innate and adaptive immune responses, resulting in both virus clearance and lung inflammation and injury. After virus clearance, resolution of ongoing inflammation and tissue repair occur during a distinct recovery period. B7 family co-stimulatory molecules such as CD80 and CD86 have important roles in modulating T cell activity during the initiation and effector stages of the host response to IAV infection, but their potential role during recovery and resolution of inflammation is unknown. We found that antibody-mediated CD86 blockade in vivo after virus clearance led to a delay in recovery, characterized by increased numbers of lung neutrophils and inflammatory cytokines in airways and lung interstitium, but no change in conventional IAV-specific T cell responses. However, CD86 blockade led to decreased numbers of FoxP3+ regulatory T cells (Tregs), and adoptive transfer of Tregs into αCD86 treated mice rescued the effect of the blockade, supporting a role for Tregs in promoting recovery after virus clearance. Specific depletion of Tregs late after infection mimicked the CD86 blockade phenotype, confirming a role for Tregs during recovery after virus clearance. Furthermore, we identified neutrophils as a target of Treg suppression since neutrophil depletion in Treg-depleted mice reduced excess inflammatory cytokines in the airways. These results demonstrate that Tregs, in a CD86 dependent mechanism, contribute to the resolution of disease after IAV infection, in part by suppressing neutrophil-driven cytokine release into the airways.
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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.