ArticleJCI insight2020
Lung group 2 innate lymphoid cells are trained by endogenous IL-33 in the neonatal period.
Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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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
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Trained innate immunity.Immunologic research · 2021Pooled it
- Group 2 innate lymphoid cells: Where are we 15 years out?The Journal of allergy and clinical immunology · 2026Review
- Fate mapping reveals a prenatal-to-neonatal wave of ILC2s with a history of Cd3g expression.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- HuR Regulates GATA3-Driven Type 2 Inflammation in CD4bioRxiv : the preprint server for biology · 2026Article
- Prenatal training grounds: the developmental origins of chronic immune disease.Journal of translational medicine · 2026Review
- Inflammatory memory: the core mechanism driving allergic asthma recurrence and chronicity.Journal of thoracic disease · 2026Review
- Single-cell analysis of recruited ILC2 cell fate during transition from circulation to establishment of tissue residency.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Early life group 2 innate lymphoid cells in health and disease.Molecular and cellular pediatrics · 2026Review
- Stem cell factor 248 shapes ILC2 transcriptional programs and promotes mucosal inflammation in allergic asthma.Frontiers in immunology · 2026Article
- Trained immunity and related memory responses in lung health and disease.Frontiers in immunology · 2026Review
- ASNS-dependent asparagine availability supports intestinal ILC2 responses and type 2 immunity under nutrient-limited conditions.Frontiers in immunology · 2026Article
- Trained immunity in chronic rhinosinusitis: epigenetic reprogramming of innate immune memory as a driver of mucosal inflammation and recurrence.Frontiers in immunology · 2026Review
- The IL-33-ILC2 axis: a key regulator of type 2 immunity in respiratory disease.Frontiers in immunology · 2026Review
- Targeting the Epithelial Alarmin Axis with Biomedical Nanoparticles: A New Frontier in Allergic Asthma Therapy.International journal of nanomedicine · 2026Review
- Multifaceted Role of ILCs in Metabolic Adaptations: From Adult to Neonate.European journal of immunology · 2025Review
- TLR4Nature communications · 2025Article
- Functional targeting of ILC2s and ILC3s reveals selective roles in intestinal fibrosis and homeostasis.The Journal of experimental medicine · 2025Article
- ILC2 Diversity, Location, and Function in Pulmonary Disease.Immunological reviews · 2025Review
- Allergen-Specific Immunotherapy and Trained Immunity.Allergy · 2025Review
- Role of Epigenetics in Chronic Lung Disease.Cells · 2025Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
Abstract
Group 2 innate lymphoid cells (ILC2s) in mouse lungs are activated by the epithelium-derived alarmin IL-33. Activated ILC2s proliferate and produce IL-5 and IL-13 that drive allergic responses. In neonatal lungs, the occurrence of spontaneous activation of lung ILC2s is dependent on endogenous IL-33. Here, we report that neonatal lung ILC2 activation by endogenous IL-33 has significant effects on ILC2 functions in adulthood. Most neonatal lung ILC2s incorporated 5-bromo-2'-deoxyuridine (BrdU) and persisted into adulthood. BrdU+ ILC2s in adult lungs responded more intensely to IL-33 treatment compared with BrdU- ILC2s. In IL-33-deficient (KO) mice, lung ILC2s develop normally, but they are not activated in the neonatal period. Lung ILC2s in KO mice responded less intensely to IL-33 in adulthood compared with WT ILC2s. While there was no difference in the number of lung ILC2s, there were fewer IL-13+ ILC2s in KO mice compared with those in WT mice. The impaired responsiveness of ILC2s in KO mice was reversed by i.n. administrations of IL-33 in the neonatal period. These results suggest that activation of lung ILC2s by endogenous IL-33 in the neonatal period may "train" ILC2s seeding the lung after birth to become long-lasting resident cells that respond more efficiently to challenges later in life.
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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.