ArticleJournal of immunology (Baltimore, Md. : 1950)2021
TLR3-Activated Monocyte-Derived Dendritic Cells Trigger Progression from Acute Viral Infection to Chronic Disease in the Lung.
Article in Journal of immunology (Baltimore, Md. : 1950), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 26 citations in OpenAlex.
- Differential regulation of monocyte exhaustion by distinct TLR agonists and underlying mechanisms.Cell communication and signaling : CCS · 2026Article
- Immune cell disorder in viral pneumonia.Journal of translational medicine · 2026Review
- Metabolic Checkpoints and Lymphoid Neogenesis in Lung Dendritic Cells: Mechanisms Guiding Tolerance and Chronic Lung Inflammation.International journal of molecular sciences · 2026Review
- Article
- Revealing roles of PANoptosis-related genes in prognosis and molecular subtypes in lung squamous cell carcinoma by integrated bioinformatic analyses and experiments.Clinical and experimental medicine · 2025Article
- Role of toll-like receptors in pulmonary immunity: mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
- Murine parainfluenza virus persists in lung innate immune cells sustaining chronic lung pathology.Nature microbiology · 2024Article
- Postinfectious Pulmonary Complications: Establishing Research Priorities to Advance the Field: An Official American Thoracic Society Workshop Report.Annals of the American Thoracic Society · 2024Review
- MAPK13 controls structural remodeling and disease after epithelial injury.bioRxiv : the preprint server for biology · 2024Article
- A correctable immune niche for epithelial stem cell reprogramming and post-viral lung diseases.The Journal of clinical investigation · 2024Article
- rWTC-MBTA Vaccine Induces Potent Adaptive Immune Responses Against Glioblastomas via Dynamic Activation of Dendritic Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Mitogen-activated protein kinase-guided drug discovery for post-viral and related types of lung disease.European respiratory review : an official journal of the European Respiratory Society · 2024Article
- The role of DC subgroups in the pathogenesis of asthma.Frontiers in immunology · 2024Review
- A potent MAPK13-14 inhibitor prevents airway inflammation and mucus production.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Murine Parainfluenza Virus Persists in Lung Innate Immune Cells Sustaining Chronic Lung Pathology.bioRxiv : the preprint server for biology · 2023Article
- A potent MAPK13-14 inhibitor prevents airway inflammation and mucus production.bioRxiv : the preprint server for biology · 2023Article
- Lung Remodeling Regions in Long-Term Coronavirus Disease 2019 Feature Basal Epithelial Cell Reprogramming.The American journal of pathology · 2023Article
- An alternative mechanism for skeletal muscle dysfunction in long-term post-viral lung disease.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- An alternative mechanism for skeletal muscle dysfunction in long-term post-viral lung disease.bioRxiv : the preprint server for biology · 2022Article
- Age-Dependent Reduction in Asthmatic Pathology through Reprogramming of Postviral Inflammatory Responses.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Acute infection is implicated as a trigger for chronic inflammatory disease, but the full basis for this switch is uncertain. In this study, we examine this issue using a mouse model of chronic lung disease that develops after respiratory infection with a natural pathogen (Sendai virus). We investigate this model using a combination of TLR3-deficient mice and adoptive transfer of immune cells into these mice versus the comparable responses in wild-type mice. We found that acute and transient expression of TLR3 on monocyte-derived dendritic cells (moDCs) was selectively required to induce long-term expression of IL-33 and consequent type 2 immune-driven lung disease. Unexpectedly, moDC participation was not based on canonical TLR3 signaling and relied instead on a trophic effect to expand the alveolar epithelial type 2 cell population beyond repair of tissue injury and thereby provide an enriched and persistent cell source of IL-33 required for progression to a disease phenotype that includes lung inflammation, hyperreactivity, excess mucus production, and remodeling. The findings thereby provide a framework wherein viral infection activates TLR3 in moDCs as a front-line immune cell niche upstream of lung epithelial cells to drive the type 2 immune response, leading to chronic inflammatory diseases of the lung (such as asthma and chronic obstructive pulmonary disease in humans) and perhaps progressive and long-term postviral disease in general.
Indexed as
Identifiers
What OpenQuestion holds
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.