ArticleJournal of immunology (Baltimore, Md. : 1950)2016
Cutting Edge: CLEC5A Mediates Macrophage Function and Chronic Obstructive Pulmonary Disease Pathologies.
Article in Journal of immunology (Baltimore, Md. : 1950), 2016. 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
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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
23 citing papers in PubMed, 36 citations in OpenAlex.
- Big data analytics for CLEC5A dynamics based on single cell genomics and proteomics reveal its diverse functions in human diseases.Nanotheranostics · 2026Article
- Macrophage spatiotemporal plasticity in pulmonary diseases: decoding the niche at single-cell resolution.Frontiers in immunology · 2026Review
- Analysis of immune characteristics and inflammatory mechanisms in COPD patients: a multi-layered study combining bulk and single-cell transcriptome analysis and machine learning.Frontiers in medicine · 2025Article
- Left atrial single-cell transcriptomics reveals amphiregulin as a surrogate marker for atrial fibrillation.Communications biology · 2024Article
- Role of sex as a biological variable in neonatal alveolar macrophages.Redox biology · 2024Article
- The influence of CLEC5A on early macrophage-mediated inflammation in COPD progression.Cellular and molecular life sciences : CMLS · 2024Article
- Macrophage Polarization and Functions in Pathogenesis of Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2024Review
- CLEC5A regulates the proliferation and migration of colon cancer via the AKT/mTOR signaling pathway.Journal of gastrointestinal oncology · 2023Article
- A Macrophage-Related Gene Signature for Identifying COPD Based on Bioinformatics and ex vivo Experiments.Journal of inflammation research · 2023Article
- CLEC5A is critical in Pseudomonas aeruginosa-induced NET formation and acute lung injury.JCI insight · 2022Article
- Microglial TYROBP/DAP12 in Alzheimer's disease: Transduction of physiological and pathological signals across TREM2.Molecular neurodegeneration · 2022Review
- Alveolar Macrophage Heterogeneity Goes up in Smoke?American journal of respiratory cell and molecular biology · 2022Article
- Airway Macrophages Encompass Transcriptionally and Functionally Distinct Subsets Altered by Smoking.American journal of respiratory cell and molecular biology · 2022Article
- Activation of the Innate Immune Checkpoint CLEC5A on Myeloid Cells in the Absence of Danger Signals Modulates Macrophages' Function but Does Not Trigger the Adaptive T Cell Immune Response.Journal of immunology research · 2022Article
- Article
- m6A RNA methylation regulators could contribute to the occurrence of chronic obstructive pulmonary disease.Journal of cellular and molecular medicine · 2020Article
- Vitamin DEBioMedicine · 2019Article
- Article
- The macrophage C-type lectin receptor CLEC5A (MDL-1) expression is associated with early plaque progression and promotes macrophage survival.Journal of translational medicine · 2017Article
- Transcriptome analysis of bronchoalveolar lavage fluid from children with severe Mycoplasma pneumoniae pneumonia reveals novel gene expression and immunodeficiency.Human genomics · 2017Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic obstructive pulmonary disease (COPD) is a devastating disease with no effective therapies. We investigated the role of the C-type lectin receptor, CLEC5A, in macrophage activation and pulmonary pathogenesis in a mouse model of COPD. We demonstrate that CLEC5A is expressed on alveolar macrophages in mice exposed long-term to cigarette smoke (CS), as well as in human smokers. We also show that CLEC5A-mediated activation of macrophages enhanced cytokine elaboration alone, as well as in combination with LPS or GM-CSF in CS-exposed mice. Furthermore, usingClec5a-deficient mice, we demonstrate that CS-induced macrophage responsiveness is mediated by CLEC5A, and CLEC5A is required for the development of inflammation, proinflammatory cytokine expression, and airspace enlargement. These findings suggest a novel mechanism that promotes airway inflammation and pathologies in response to CS exposure and identifies CLEC5A as a novel target for the therapeutic control of COPD pathogenesis.
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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.