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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.

Keywords:

Atopic dermatitis IL-22 IL-22RA1 skin inflammation temtokibart treatment

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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.