ArticleMucosal immunology2020
Long-lived regulatory T cells generated during severe bronchiolitis in infancy influence later progression to asthma.
Article in Mucosal immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- Early-life immune imprinting by a B. infantis-HMO synbiotic shapes infant immune signatures and protects against experimental respiratory disease.Cell reports. Medicine · 2026Article
- IL-27-DependentInternational journal of molecular sciences · 2026Article
- The potential role of n-3 fatty acids and their lipid mediators on asthmatic airway inflammation.Frontiers in immunology · 2024Review
- The role of DC subgroups in the pathogenesis of asthma.Frontiers in immunology · 2024Review
- Regulatory T cells in lung disease and transplantation.Bioscience reports · 2023Review
- Gut microecological regulation on bronchiolitis and asthma in children: A review.The clinical respiratory journal · 2023Review
- Respiratory syncytial virus infection during infancy and asthma during childhood in the USA (INSPIRE): a population-based, prospective birth cohort study.Lancet (London, England) · 2023Article
- Hosts, microbiomes, and the evolution of critical windows.Evolution letters · 2022Article
- T-cell responses in asthma exacerbations.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2022Review
- Serum periostin among infants with severe bronchiolitis and risk of developing asthma: A prospective multicenter cohort study.Allergy · 2022Article
- Gut Microbiome and Metabolomics Profiles of Allergic and Non-Allergic Childhood Asthma.Journal of asthma and allergy · 2022Article
- Effect of Infant RSV Infection on Memory T Cell Responses at Age 2-3 Years.Frontiers in immunology · 2022Article
- Modulation of Vagal Sensory NeuronsFrontiers in physiology · 2021Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The type-2 inflammatory response that promotes asthma pathophysiology occurs in the absence of sufficient immunoregulation. Impaired regulatory T cell (Treg) function also predisposes to severe viral bronchiolitis in infancy, a major risk factor for asthma. Hence, we hypothesized that long-lived, aberrantly programmed Tregs causally link viral bronchiolitis with later asthma. Here we found that transient plasmacytoid dendritic cell (pDC) depletion during viral infection in early-life, which causes the expansion of aberrant Tregs, predisposes to allergen-induced or virus-induced asthma in later-life, and is associated with altered airway epithelial cell (AEC) responses and the expansion of impaired, long-lived Tregs. Critically, the adoptive transfer of aberrant Tregs (unlike healthy Tregs) to asthma-susceptible mice failed to prevent the development of viral-induced or allergen-induced asthma. Lack of protection was associated with increased airway epithelial cytoplasmic-HMGB1 (high-mobility group box 1), a pro-type-2 inflammatory alarmin, and granulocytic inflammation. Aberrant Tregs expressed lower levels of CD39, an ectonucleotidase that hydrolyzes extracellular ATP, a known inducer of alarmin release. Using cultured mouse AECs, we identify that healthy Tregs suppress allergen-induced HMGB1 translocation whereas this ability is markedly impaired in aberrant Tregs. Thus, defective Treg programming in infancy has durable consequences that underlie the association between bronchiolitis and subsequent asthma.
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