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Updated: Aug 14, 2025

Isolation and Culture of Primary Mouse Keratinocytes from Neonatal and Adult Mouse Skin
Published on: July 14, 2017
Keratinocytes activated by IL-4/IL-13 express IL-2Rγ with consequences on epidermal barrier function
Audrey Progneaux1, Céline Evrard1, Valérie De Glas1
1Research Unit of Molecular Physiology (URPhyM), NAmur Research Institute for LIfe Sciences (NARILIS), University of Namur, Namur, Belgium.
Interleukin-2 receptor gamma (IL-2Rγ) is induced in skin cells by atopic dermatitis (AD) triggers, contributing to epidermal barrier dysfunction and regulating other inflammatory signals.
Area of Science:
- Dermatology
- Immunology
- Cell Biology
Background:
- Atopic dermatitis (AD) involves Th2 inflammation and epidermal barrier defects.
- Interleukin-4 (IL-4) and Interleukin-13 (IL-13) cytokines mediate AD pathogenesis.
- The role of IL-2 receptor gamma (IL-2Rγ) in keratinocytes is not fully understood.
Purpose of the Study:
- To investigate IL-2Rγ expression in keratinocytes.
- To determine the role of IL-2Rγ in epidermal barrier function.
- To elucidate the mechanism of IL-2Rγ induction in AD.
Main Methods:
- Utilized reconstructed human epidermis (RHE) models and lesional AD skin.
- Analyzed IL-2Rγ expression via mRNA and protein levels.
- Employed JAK inhibitors and CRISPR-Cas9 gene editing (IL13RA1 and IL2RG knockouts).
Main Results:
- IL-4 and IL-13 induce IL-2Rγ expression in RHE and AD skin keratinocytes.
- IL-2Rγ induction is mediated by the type II receptor pathway (IL-4Rα/IL-13Rα1).
- IL-2Rγ deficiency prevents IL-4/IL-13-induced epidermal barrier disruption and alters IL-13Rα2 expression.
Conclusions:
- Keratinocyte IL-2Rγ is induced via the type II receptor and contributes to AD-related skin barrier issues.
- IL-2Rγ plays a role in regulating IL-13Rα2 expression.
- IL-2Rγ is a potential therapeutic target for atopic dermatitis.
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