ArticleThe Journal of clinical investigation2021
Basal epithelial stem cells cross an alarmin checkpoint for postviral lung disease.
Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 51 citations in OpenAlex.
- Dysplastic Epithelial Repair Propagates Chronic Pathology Through the Paracrine Transformation of Pulmonary Fibroblasts.bioRxiv : the preprint server for biology · 2026Article
- RelA Signaling inInternational journal of molecular sciences · 2026Article
- Airway epithelial heterogeneity and mucus plugging in asthmatic bronchioles.American journal of respiratory and critical care medicine · 2026Article
- Fibroblast-derived alarmin promotes oral wound healing by activating regulatory T cells that relay pro-angiogenic and anti-inflammatory responses.Cell reports · 2026Article
- Divergent aging of nulliparous and parous mammary glands reveals IL33+ hybrid epithelial cells.Nature communications · 2026Article
- IRF1 mediates airway epithelial innate memory through priming BRD4- EP300 activity.Frontiers in immunology · 2026Article
- Lineage Tracing of Distal Lung Epithelial Progenitors in Injury-Induced Regeneration.The clinical respiratory journal · 2025Review
- Tolerogenic lung allograft microenvironment suppresses pathogenic tissue remodeling following respiratory virus infection in mice.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2025Article
- The long reach of influenza and other respiratory viruses: from acute epithelial injury to post-viral lung disease.Clinical microbiology reviews · 2025Review
- Advances in Single-Cell Sequencing for Infectious Diseases: Progress and Perspectives.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- SMARCA4 regulates inducible BRD4 genomic redistribution coupling intrinsic immunity and plasticity in epithelial injury-repair.Nucleic acids research · 2025Article
- Respiratory long COVID in aged hamsters features impaired lung function post-exercise with bronchiolization and fibrosis.Nature communications · 2025Article
- Therapeutic targeting of full-length interleukin-33 protein levels with cell-permeable decoy peptides attenuates fibrosis in the bleomycin model in vivo.The Journal of pharmacology and experimental therapeutics · 2025Article
- Innovation through imitation: IL-33 decoys show promise in pulmonary fibrosis.The Journal of pharmacology and experimental therapeutics · 2025Article
- MrgprA3 neurons drive cutaneous immunity against helminths through selective control of myeloid-derived IL-33.Nature immunology · 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
- The post-viral GPNMBmedRxiv : the preprint server for health sciences · 2024Article
- MAPK13 controls structural remodeling and disease after epithelial injury.bioRxiv : the preprint server for biology · 2024Article
- IL-33: Friend or foe in transplantation?The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2024Review
- A correctable immune niche for epithelial stem cell reprogramming and post-viral lung diseases.The Journal of clinical investigation · 2024Article
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18 authors at 3 institutions in 1 country.
Funding
Abstract
Epithelial cells are charged with protection at barrier sites, but whether this normally beneficial response might sometimes become dysfunctional still needs definition. Here, we recognized a pattern of imbalance marked by basal epithelial cell growth and differentiation that replaced normal airspaces in a mouse model of progressive postviral lung disease due to the Sendai virus. Single-cell and lineage-tracing technologies identified a distinct subset of basal epithelial stem cells (basal ESCs) that extended into gas-exchange tissue to form long-term bronchiolar-alveolar remodeling regions. Moreover, this cell subset was selectively expanded by crossing a cell-growth and survival checkpoint linked to the nuclear-localized alarmin IL-33 that was independent of IL-33 receptor signaling and instead connected to autocrine chromatin accessibility. This mechanism creates an activated stem-progenitor cell lineage with potential for physiological or pathological function. Thus, conditional loss of Il33 gene function in basal epithelial cells disrupted the homeostasis of the epithelial barrier at skin and gut sites but also markedly attenuated postviral disease in the lung based on the downregulation of remodeling and inflammation. Thus, we define a basal ESC strategy to deploy innate immune machinery that appears to overshoot the primordial goal of self-defense. Our findings reveal new targets to stratify and correct chronic and often deadly postviral disease.
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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.