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Updated: Aug 30, 2025
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Isolation of Group 2 Innate Lymphoid Cells from Mouse Nasal Mucosa to Detect the Expression of CD226
Published on: May 10, 2022
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[Pathogenic changes in group 2 innate lymphoid cells (ILC2) in intractable asthma]
1Laboratory of Immunopharmacology, Faculty of Pharmaceutical Sciences, Setsunan University.
Nihon Yakurigaku Zasshi. Folia Pharmacologica Japonica
|September 1, 2022
Summary
Steroid-resistant asthma involves pathogenic type 2 innate lymphoid cells (ILC2). These cells produce excess cytokines, contributing to steroid insensitivity in asthma models, suggesting new therapeutic targets.
Area of Science:
- Immunology
- Pulmonology
- Cell Biology
Background:
- A significant portion of asthma patients exhibit steroid resistance, posing a clinical challenge.
- The underlying mechanisms of steroid-insensitive asthma remain poorly understood due to limited suitable models.
Purpose of the Study:
- To investigate the role of type 2 innate lymphoid cells (ILC2) in a newly developed steroid-resistant asthma model.
- To elucidate the molecular mechanisms contributing to steroid insensitivity in asthma.
Main Methods:
- Development of a steroid-insensitive asthma model in BALB/c mice using high-dose ovalbumin challenge.
- In vitro stimulation of Th2 cells and ILC2 to compare cytokine production.
- Analysis of thymic stromal lymphopoietin (TSLP) receptor and STAT5a gene expression in ILC2.
- Assessment of therapeutic effects of anti-IL-5 antibody on steroid sensitivity.
Main Results:
- High-dose ovalbumin challenge induced steroid-insensitive airway inflammation and remodeling.
- Lung ILC2 from the steroid-insensitive model produced significantly higher levels of type 2 cytokines compared to steroid-sensitive models.
- ILC2 in the steroid-insensitive model showed increased expression of TSLP receptor and STAT5a.
- Treatment with anti-IL-5 antibody restored steroid sensitivity in the asthma model.
Conclusions:
- Type 2 innate lymphoid cells (ILC2) play a pathogenic role in steroid-resistant asthma.
- ILC2-derived interleukin-5 (IL-5) overproduction may drive steroid resistance.
- Targeting ILC2-related molecules offers potential for novel therapeutic strategies for intractable asthma.
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