ArticleAllergy2018
ILC2 frequency and activity are inhibited by glucocorticoid treatment via STAT pathway in patients with asthma.
Article in Allergy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
What it found
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Who cites it
59 citing papers in PubMed, 94 citations in OpenAlex.
- Group 2 innate lymphoid cells: Where are we 15 years out?The Journal of allergy and clinical immunology · 2026Review
- Ginsenoside Rg5 alleviates allergic rhinitis in rats by modulating nasal microbiota by inhibiting JAK2/STAT3/BCL-2 and MAPK signaling.Journal of ginseng research · 2026Article
- Acute stress alleviates type 2 lung inflammation by restricting ILC2s through corticosterone-glucocorticoid receptor signaling.Cellular & molecular immunology · 2026Article
- Interleukin-Mediated Macrophage Polarization in Allergic Rhinitis Inflammation: A Systematic Review.Journal of inflammation research · 2026Review
- Stem cell factor 248 shapes ILC2 transcriptional programs and promotes mucosal inflammation in allergic asthma.Frontiers in immunology · 2026Article
- The shifting balance: innate lymphoid cell plasticity in chronic gut diseases.Frontiers in immunology · 2026Review
- CPA3 drives the development of asthma by promoting the activation of the JAK/STAT6 pathway.Respiratory research · 2025Article
- Mesenchymal stem cell-derived exosomes: a new hope for improving asthma airway remodeling.Annals of medicine · 2025Review
- ILC2 Diversity, Location, and Function in Pulmonary Disease.Immunological reviews · 2025Review
- Decoding innate lymphoid cells and innate-like lymphocytes in asthma: pathways to mechanisms and therapies.Journal of biomedical science · 2025Review
- Role of ILC2s as Potential Effector Cells of IL25-Mediated Type 2 Inflammation in Chronic Rhinosinusitis with Nasal Polyps in China.Journal of inflammation research · 2025Article
- Physiopathological Roles of White Adiposity and Gut Functions in Neuroinflammation.International journal of molecular sciences · 2024Review
- Expression of Epithelial Alarmin Receptor on Innate Lymphoid Cells Type 2 in Eosinophilic Chronic Obstructive Pulmonary Disease.Advances in respiratory medicine · 2024Article
- TNF Superfamily and ILC2 Activation in Asthma.Biomolecules · 2024Review
- JAK3 inhibitor suppresses multipotent ILC2s and attenuates steroid-resistant asthma.Science advances · 2023Article
- Role of IL-33-ST2 pathway in regulating inflammation: current evidence and future perspectives.Journal of translational medicine · 2023Review
- Induction of a type 2 inflammatory chronic rhinosinusitis in C57BL/6 mice.Asia Pacific allergy · 2023Article
- The modulation of pulmonary group 2 innate lymphoid cell function in asthma: from inflammatory mediators to environmental and metabolic factors.Experimental & molecular medicine · 2023Review
- Dendritic cells mediated by small extracellular vesicles derived from MSCs attenuated the ILC2 activity via PGE2 in patients with allergic rhinitis.Stem cell research & therapy · 2023Article
- HTR2A agonists play a therapeutic role by restricting ILC2 activation in papain-induced lung inflammation.Cellular & molecular immunology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGroup 2 innate lymphoid cells (ILC2s) were closely associated with asthma. However, there were no perspective studies about the effects of glucocorticoid on ILC2s in asthma patients. Our objective was to perform a perspective study and evaluate the ILC2 activity after glucocorticoid therapy in asthma patients.
methodsThe asthma and asthma with allergic rhinitis patients were treated with glucocorticoid for 3 months. The circulating ILC2 levels were evaluated. The effects of glucocorticoid on ILC2s and possible signalling pathways were investigated in vitro.
resultsThe patients were well-controlled, and the high ILC2 levels were significantly decreased at 1 and 3 months after treatment. Peripheral blood monocytes from allergic patients produced dramatic IL-5, IL-13 and IL-9 in response to IL-25, IL-33 plus IL-2, and glucocorticoid significantly decreased their levels. Moreover, ILC2s were identified to be the predominant source of IL-5, IL-13 and IL-9, and glucocorticoid treatment was able to reverse their high levels. STAT3, STAT5, STAT6, JAK3 and MEK signalling pathways were proved to be involved in regulating ILC2 activity under the glucocorticoid treatment.
conclusionThe data suggested that glucocorticoid administration could be effective in treating asthma by regulating ILC2s via MEK/JAK-STAT signalling pathways. This provides a new understanding of glucocorticoid application in regard to allergic diseases.
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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.