ArticleFrontiers in allergy2022
IL-33 induces NF-κB activation in ILC2 that can be suppressed by
Article in Frontiers in allergy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Alleviation of Chitin- and Ovalbumin-Induced Steroid-Resistant Eosinophilic Airway Inflammation Associated with NLRP3 Axis Inhibition in a Mouse Model.Journal of inflammation research · 2026Article
- Hormone-dependent immune regulation shapes asthma heterogeneity across the female lifespan.Frontiers in immunology · 2026Review
- Regulating Neutrophilic Asthma with IL-33: Maybe We Shouldn't Block IL-33 after All?American journal of respiratory cell and molecular biology · 2025Article
- Current Understanding of Epithelial-Derived Alarmins in Chronic Rhinosinusitis with Nasal Polyps.Clinical reviews in allergy & immunology · 2025Review
- Serum 17Frontiers in immunology · 2025Article
- Single-Cell Analysis: A Method for In-Depth Phenotyping of Cells Involved in Asthma.International journal of molecular sciences · 2024Review
- SIRPα engagement regulates ILC2 effector function and alleviates airway hyperreactivity via modulating energy metabolism.Cellular & molecular immunology · 2024Article
- Progesterone amplifies allergic inflammation and airway pathology in association with higher lung ILC2 responses.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Targeting NF-κB Signaling: Selected Small Molecules Downregulate Pro-Inflammatory Cytokines in Both Food Allergen and LPS-Induced Inflammation.International journal of molecular sciences · 2024Article
- The causal relationship between multiple autoimmune diseases and nasal polyps.Frontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Asthmatic women tend to develop severe airway disease in their reproductive years, and 30%-40% of asthmatic women have peri-menstrual worsening of asthma symptoms. This indicates that fluctuations in ovarian hormones are involved in advancement of asthmatic disease and exacerbation of symptoms. Group 2 innate lymphoid cells, or ILC2, are readily detected in allergic conditions, such as rhinosinusitis, in individuals that develop nasal polyps do to allergen exposures, and in allergic asthma. ILC2 are airway localized immune cells activated by IL-33, an innate cytokine that perpetuates allergic inflammation by driving the production of IL-5 and IL-13. We have previously shown that ILC2 are highly activated in naïve and ovalbumin (OVA) challenged, female BALB/c mice in comparison to male mice following stimulation with IL-33. Here, we investigated the effect of steady-state ovarian hormones on ILC2 and the NF-κB signaling pathway following OVA sensitization and challenge. We found that estrogen-treated ovariectomized mice (OVX-E2) that had been challenged with OVA had reduced IL-5 and IL-13 production by lung ILC2 as compared to lung ILC2 isolated from intact male and female sham-operated controls that had been treated with OVA. ILC2 were isolated from untreated animals and co-cultured
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