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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.

Experimental Dermatology
|January 16, 2023
PubMed
Summary

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.

Keywords:
Signal Transduction.atopic dermatitisbarrier functioninterleukinskeratinocyte biology

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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.