ArticleFrontiers in immunology2023
CC16 drives VLA-2-dependent SPLUNC1 expression.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 6 citations in OpenAlex.
- Impaired CC16-mediated host responses to rhinovirus in nasal epithelial cells from patients with asthma.The Journal of allergy and clinical immunology · 2026Article
- Maternal smoking and CC-16: implications for lung development and COPD across the lifespan.American journal of respiratory and critical care medicine · 2026Article
- The role of CC16 in the associations of preterm birth with lung function and asthma in adult life.The Journal of allergy and clinical immunology · 2026Article
- From respiratory infections to environmental exposures: CC16 is a key modulator of airway homeostasis.Frontiers in medicine · 2026Review
- Genome-wide Association Study IdentifiesAllergy, asthma & immunology research · 2026Article
- Article
- Investigation of lactotransferrin messenger RNA expression levels as an anti-type 2 asthma biomarker.The Journal of allergy and clinical immunology · 2024Article
Corrections and comments
- Comment on
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Rationale: CC16 (Club Cell Secretory Protein) is a protein produced by club cells and other non-ciliated epithelial cells within the lungs. CC16 has been shown to protect against the development of obstructive lung diseases and attenuate pulmonary pathogen burden. Despite recent advances in understanding CC16 effects in circulation, the biological mechanisms of CC16 in pulmonary epithelial responses have not been elucidated. Objectives: We sought to determine if CC16 deficiency impairs epithelial-driven host responses and identify novel receptors expressed within the pulmonary epithelium through which CC16 imparts activity. Methods: We utilized mass spectrometry and quantitative proteomics to investigate how CC16 deficiency impacts apically secreted pulmonary epithelial proteins. Mouse tracheal epithelial cells (MTECS), human nasal epithelial cells (HNECs) and mice were studied in naïve conditions and after Mp challenge. Measurements and main results: We identified 8 antimicrobial proteins significantly decreased by CC16 Conclusion: Our findings demonstrate a novel role for CC16 in epithelial-driven host defense by up-regulating antimicrobials and define a novel epithelial receptor for CC16, VLA-2, through which signaling is necessary for enhanced SPLUNC1 production.
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.