ArticleClinical and translational allergy2023
Interleukin-33 increases type 2 innate lymphoid cell count and their activation in eosinophilic asthma.
Article in Clinical and translational allergy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Review
- Platelet-mast cell dialogue in innate immune response and inflammation.American journal of physiology. Lung cellular and molecular physiology · 2026Review
- Nuclear IL-33 amplifies NF-κB signaling to drive neutrophil recruitment and activation in the endocervical epithelium duringFrontiers in immunology · 2026Article
- The Major Role of Type 2 Inflammation in Asthma: From the Perspective of Immunological Mechanism.BioMed research international · 2026Review
- Stem cell factor 248 shapes ILC2 transcriptional programs and promotes mucosal inflammation in allergic asthma.Frontiers in immunology · 2026Article
- Role of IL-5 in eosinophil-associated diseases and prospects for multi-target therapy.Frontiers in immunology · 2026Review
- Current Understanding of Epithelial-Derived Alarmins in Chronic Rhinosinusitis with Nasal Polyps.Clinical reviews in allergy & immunology · 2025Review
- Interleukin-33 increases type 2 innate lymphoid cell count and their activation in eosinophilic asthma.Clinical and translational allergy · 2023Article
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16 authors at 1 institution in 1 country.
Funding
Abstract
backgroundInterleukin-33 (IL-33) exacerbates asthma probably through type 2 innate lymphoid cells (ILC2s). Nevertheless, the association between eosinophilic asthma (EA) and ILC2s remains obscure, and the mechanisms by which IL-33 affects ILC2s are yet to be clarified.
methodsILC2s were evaluated in peripheral blood mononuclear cells, induced sputum, and bronchoalveolar lavage fluid obtained from patients with EA. Confocal microscopy was performed to locate ILC2s in lung tissue and the mRNA expression of ILC2-related genes was also evaluated in the EA model. The proliferation of ILC2s isolated from humans and mice was assessed following IL-33 or anti-IL-33 stimulation.
resultsThe counts, activation, and mRNA expression of relevant genes in ILC2s were higher in PBMCs and airways of patients with EA. In addition, ILC2 cell counts correlated with Asthma control test, blood eosinophil count, Fractional exhaled nitric oxide level, and predicted eosinophilic airway inflammation. IL-33 induced stronger proliferation of ILC2s and increased their density around blood vessels in the lungs of mice with EA. Moreover, IL-33 treatment increased the counts and activation of ILC2s and lung inflammatory scores, whereas anti-IL-33 antibody significantly reversed these effects in EA mice. Finally, IL-33 enhanced PI3K and AKT protein expression in ILC2s, whereas inhibition of the PI3K/AKT pathway decreased IL-5 and IL-13 production by ILC2s in EA.
conclusionsILC2s, especially activated ILC2s, might be critical markers of EA. IL-33 can induce and activate ILC2s in the lungs via the PI3K/AKT pathway in EA. Thus, using anti-IL-33 antibody could be a part of an effective treatment strategy for EA.
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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 Socratic graph.