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Neutralizing IL-22RA1 improves histologic and molecular alterations associated with atopic dermatitis pathogenesis
Sophia Wasserer1, Thomas Litman2, Josephine Hebsgaard2
1Department of Dermatology and Allergy, Technical University of Munich, Munich, Germany.
The Journal of Allergy and Clinical Immunology
|November 13, 2025
Summary
Blocking the IL-22/IL-22 receptor (IL-22RA1) axis shows therapeutic potential for atopic dermatitis (AD). This study found IL-22RA1 contributes to AD pathogenesis and its inhibition improves skin barrier integrity in models.
Area of Science:
- Dermatology
- Immunology
- Molecular Biology
Background:
- Atopic dermatitis (AD) is a heterogeneous inflammatory skin disease.
- Some patients with AD show poor response to existing systemic therapies.
- Novel therapeutic targets are needed for AD treatment.
Purpose of the Study:
- To investigate the role of the IL-22/IL-22 receptor (IL-22RA1) axis in AD skin inflammation.
- To evaluate the therapeutic potential of blocking the IL-22/IL-22RA1 axis in AD.
Main Methods:
- Assessed IL22RA1 expression in AD skin via in situ hybridization.
- Evaluated IL-22/IL-22R signaling inhibition using temtokibart (anti-IL-22RA1 antibody).
- Utilized in vitro (3-D skin equivalents) and in vivo (TPA mouse model) AD models.
Main Results:
- IL22RA1 expression was elevated in lesional AD skin, correlating with epidermal thickness.
- IL-22 stimulation in 3-D skin equivalents induced AD-like molecular signatures.
- Temtokibart treatment improved skin barrier integrity and reduced inflammatory markers in models.
Conclusions:
- The IL-22/IL-22RA1 axis plays a functional role in AD pathogenesis.
- Blocking IL-22RA1 is a promising therapeutic strategy for AD.
