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IL-33 and ST2 in atopic dermatitis: expression profiles and modulation by triggering factors
Terhi Savinko1, Sampsa Matikainen, Ulpu Saarialho-Kere
1Unit of Immunotoxicology, Finnish Institute of Occupational Health, Helsinki, Finland.
The Journal of Investigative Dermatology
|January 27, 2012
Summary
Interleukin-33 (IL-33) and its receptor ST2 are upregulated in atopic dermatitis (AD) skin, suggesting a key role in the inflammatory skin condition. Their expression is influenced by various triggers and suppressed by tacrolimus.
Area of Science:
- Immunology
- Dermatology
- Molecular Biology
Background:
- Atopic dermatitis (AD) involves T-helper type 2 (Th2) cytokine-driven skin inflammation.
- Interleukin-33 (IL-33) is a cytokine produced by barrier tissues that activates Th2 lymphocytes, mast cells, and eosinophils.
- IL-33 signaling occurs via a receptor complex including ST2 and IL-1RAcP.
Purpose of the Study:
- To investigate the expression of IL-33 and its receptor components (ST2, IL-1RAcP) in human AD skin and relevant models.
- To explore the cellular sources and regulation of IL-33 production in skin.
- To assess the impact of topical tacrolimus on IL-33/ST2 expression in AD.
Main Methods:
- Analysis of IL-33 and ST2 expression in human AD skin biopsies.
- Examination of IL-33/ST2 in a murine model of AD (filaggrin-deficient mice).
- In vitro studies using skin fibroblasts, keratinocytes, macrophages, and endothelial cells to assess IL-33 production.
- Evaluation of the effect of topical tacrolimus on IL-33/ST2 expression.
Main Results:
- Increased expression of IL-33 and ST2 was observed in human AD skin following allergen or staphylococcal enterotoxin B (SEB) exposure.
- Elevated IL-33 and ST2 levels were found in the skin of filaggrin-deficient mice, a model for AD.
- Fibroblasts, keratinocytes, macrophages, and endothelial cells produced IL-33 upon stimulation with TNF-α, IFN-γ, and double-stranded RNA.
- Topical tacrolimus treatment reduced the increased expression of IL-33 and ST2 induced by irritants, allergens, or SEB.
Conclusions:
- The IL-33/ST2 interaction plays a significant role in the pathogenesis of atopic dermatitis.
- Bacterial and viral infections may contribute to increased IL-33 production in AD.
- Targeting the IL-33/ST2 pathway could be a potential therapeutic strategy for AD.
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