ArticleNature communications2022
Cigarette smoke aggravates asthma by inducing memory-like type 3 innate lymphoid cells.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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
19 citing papers in PubMed, 35 citations in OpenAlex.
- Type 2-low Asthma: Epidemiology, Multiomics, and Emerging Therapies.Current allergy and asthma reports · 2026Review
- Erythromycin inhibits the differentiation of NCRJournal of thoracic disease · 2026Article
- Impacts of Environmental Pollutants on Innate Immunity: The Role of Group 2 Innate Lymphoid Cells.Clinical reviews in allergy & immunology · 2026Review
- Emerging Therapeutic Strategies in Asthma: Advances in Treatment, Drug Delivery, Drug Adherence, and Disease Management.Current allergy and asthma reports · 2026Review
- USP18 confers protection against allergic asthma by suppressing CCL8 production in alveolar type II epithelial cells.Respiratory research · 2025Article
- Decoding innate lymphoid cells and innate-like lymphocytes in asthma: pathways to mechanisms and therapies.Journal of biomedical science · 2025Review
- Chronic Inflammation in Asthma: Looking Beyond the Th2 Cell.Immunological reviews · 2025Review
- Exploring the pathogenesis and clinical implications of asthma, chronic obstructive pulmonary disease (COPD), and asthma-COPD overlap (ACO): a narrative review.Frontiers in medicine · 2025Review
- Identification of Novel Biomarkers Associated with Corticosteroid Resistance in Asthma by Bioinformatics Analysis and Experimental Validation.Journal of inflammation research · 2025Article
- Group 3 Innate Lymphoid Cells: A Potential Therapeutic Target for Steroid Resistant Asthma.Clinical reviews in allergy & immunology · 2024Review
- Dissecting the pathogenic effects of smoking in blood DNA methylation on allergic diseases.The World Allergy Organization journal · 2024Article
- Contribution of IL-17C-mediated macrophage polarization to Type 17 inflammation in neutrophilic asthma.Cell communication and signaling : CCS · 2024Article
- Article
- Advances in non-type 2 severe asthma: from molecular insights to novel treatment strategies.The European respiratory journal · 2024Review
- Antioxidant Intake and Biomarkers of Asthma in Relation to Smoking Status-A Review.Current issues in molecular biology · 2023Review
- Workup of difficult-to-treat asthma: implications from treatable traits.Precision clinical medicine · 2023Article
- Special Issue on 'Asthma and Allergic Inflammation'.Vaccines · 2023Article
- ILC3: a case of conflicted identity.Frontiers in immunology · 2023Review
- Memory-like innate lymphoid cells in the pathogenesis of asthma.Frontiers in immunology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although cigarette smoking is known to exacerbate asthma, only a few clinical asthma studies have been conducted involving smokers. Here we show, by comparing paired sputum and blood samples from smoking and non-smoking patients with asthma, that smoking associates with significantly higher frequencies of pro-inflammatory, natural-cytotoxicity-receptor-non-expressing type 3 innate lymphoid cells (ILC3) in the sputum and memory-like, CD45RO-expressing ILC3s in the blood. These ILC3 frequencies positively correlate with circulating neutrophil counts and M1 alveolar macrophage frequencies, which are known to increase in uncontrolled severe asthma, yet do not correlate with circulating eosinophil frequencies that characterize allergic asthma. In vitro exposure of ILCs to cigarette smoke extract induces expression of the memory marker CD45RO in ILC3s. Cigarette smoke extract also impairs the barrier function of airway epithelial cells and increases their production of IL-1β, which is a known activating factor for ILC3s. Thus, our study suggests that cigarette smoking increases local and circulating frequencies of activated ILC3 cells, plays a role in their activation, thereby aggravating non-allergic inflammation and the severity of asthma.
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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.