ArticleCell reports2024
Prenatal inflammation remodels lung immunity and function by programming ILC2 hyperactivation.
Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Prenatal training grounds: the developmental origins of chronic immune disease.Journal of translational medicine · 2026Review
- Environmental factors that regulate host-helminth interactions.Trends in parasitology · 2026Review
- Single-Cell Atlas of Fetal Immune Development Across Lung, Spleen, and Umbilical Cord Blood in Nonhuman Primates.Research square · 2026Article
- Early life group 2 innate lymphoid cells in health and disease.Molecular and cellular pediatrics · 2026Review
- The epigenetic-immune-microbiome axis in early life: reprogramming the origins and endotypes of pediatric asthma.Frontiers in immunology · 2026Review
- Developmental Impact of Maternal Immune Activation on the Fetal Immune System and Lung.European journal of immunology · 2026Review
- Impact of maternal visceral leishmaniasis on sex-specific immune responses and pathogenesis in offspring following homologous infections.Frontiers in immunology · 2026Article
- When stress exceeds developmental capacity: rethinking cell death in bronchopulmonary dysplasia.Frontiers in pediatrics · 2026Article
- Immune evasion of multidrug-resistant bacteria: insights from lung innate immune cells and targeted therapies.Frontiers in cellular and infection microbiology · 2026Review
- Maternal IgE Influence on Fetal and Infant Health.Immunological reviews · 2025Review
- Chronic Inflammation in Asthma: Looking Beyond the Th2 Cell.Immunological reviews · 2025Review
- The impact of vitamin D on atopic disorders: assessing evidence for a causal relationship.Frontiers in nutrition · 2025Article
- H3K27me3 modulates trained immunity of monocytes in HDM-allergic diseases.Frontiers in immunology · 2025Article
- Carnosine as a protective metabolic mediator in inflammatory lung injury by inhibiting macrophage infiltration and M1-like polarization.Frontiers in pharmacology · 2025Article
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Authors and funding
8 authors.
Funding
Abstract
Here, we examine how prenatal inflammation shapes tissue function and immunity in the lung by reprogramming tissue-resident immune cells from early development. Maternal, but not fetal, type I interferon-mediated inflammation provokes expansion and hyperactivation of group 2 innate lymphoid cells (ILC2s) seeding the developing lung. Hyperactivated ILC2s produce increased IL-5 and IL-13 and are associated with acute Th2 bias, decreased Tregs, and persistent lung eosinophilia into adulthood. ILC2 hyperactivation is recapitulated by adoptive transfer of fetal liver precursors following prenatal inflammation, indicative of developmental programming at the fetal progenitor level. Reprogrammed ILC2 hyperactivation and subsequent lung immune remodeling, including persistent eosinophilia, is concomitant with worsened histopathology and increased airway dysfunction equivalent to papain exposure, indicating increased asthma susceptibility in offspring. Our data elucidate a mechanism by which early-life inflammation results in increased asthma susceptibility in the presence of hyperactivated ILC2s that drive persistent changes to lung immunity during perinatal development.
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