ArticleJCI insight2017
Prolonged activation of IL-5-producing ILC2 causes pulmonary arterial hypertrophy.
Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- The association between soluble ST2 and transplant-free survival in precapillary pulmonary hypertension.JHLT open · 2026Article
- Basic implications on three pathways associated with SARS-CoV-2.Biomedical journal · 2025Review
- Article
- Eosinophils protect against pulmonary hypertension through 14-HDHA and 17-HDHA.The European respiratory journal · 2023Article
- Two cases of pulmonary arterial hypertension with specific vascular Мalformations and unique eosinophilic inflammation in carriers of theRespiratory medicine case reports · 2023Article
- Prostacyclin Regulation of Allergic Inflammation.Biomedicines · 2022Review
- Heartbreakers or Healers? Innate Lymphoid Cells in Cardiovascular Disease and Obesity.Frontiers in immunology · 2022Review
- Heterogeneity of Group 2 Innate Lymphoid Cells Defines Their Pleiotropic Roles in Cancer, Obesity, and Cardiovascular Diseases.Frontiers in immunology · 2022Review
- COX Inhibition IncreasesJournal of immunology (Baltimore, Md. : 1950) · 2020Article
- Contributions of IL-33 in Non-hematopoietic Lung Cells to Obstructive Lung Disease.Frontiers in immunology · 2020Review
- M2-like macrophages serve as a niche for adipocyte progenitors in adipose tissue.Journal of diabetes investigation · 2019Review
- Neuropeptide CGRP Limits Group 2 Innate Lymphoid Cell Responses and Constrains Type 2 Inflammation.Immunity · 2019Article
- IL-33 Initiates Vascular Remodelling in Hypoxic Pulmonary Hypertension by up-Regulating HIF-1α and VEGF Expression in Vascular Endothelial Cells.EBioMedicine · 2018Article
- A meta-analysis of soluble suppression of tumorigenicity 2 (sST2) and clinical outcomes in pulmonary hypertension.Journal of geriatric cardiology : JGC · 2017Article
- Functions of tissue-resident eosinophils.Nature reviews. Immunology · 2017Review
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
IL-33 is one of the critical cytokines that activates group 2 innate lymphoid cells (ILC2s) and mediates allergic reactions. Accumulating evidence suggests that IL-33 is also involved in the pathogenesis of several chronic inflammatory diseases. Previously, we generated an IL-5 reporter mouse and revealed that lung IL-5-producing ILC2s played essential roles in regulating eosinophil biology. In this study, we evaluated the consequences of IL-33 administration over a long period, and we observed significant expansion of ILC2s and eosinophils surrounding pulmonary arteries. Unexpectedly, pulmonary arteries showed severe occlusive hypertrophy that was ameliorated in IL-5- or eosinophil-deficient mice, but not in Rag2-deficient mice. This indicates that IL-5-producing ILC2s and eosinophils play pivotal roles in pulmonary arterial hypertrophy. Administration of a clinically used vasodilator was effective in reducing IL-33-induced hypertrophy and repressed the expansion of ILC2s and eosinophils. Taken together, these observations demonstrate a previously unrecognized mechanism in the development of pulmonary arterial hypertrophy and the causative roles of ILC2 in the process.
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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.