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The OX40/OX40L Axis Promotes Th2 Activity and Impairs Regulatory T Cell Function in Atopic Dermatitis
Kazuhiko Yamamura1, Dante Dahabreh2, Ester Del Duca2,3
1Laboratory of Investigative Dermatology, The Rockefeller University, New York, New York, USA.
Allergy
|March 7, 2026
Summary
The OX40/OX40L axis promotes atopic dermatitis (AD) inflammation by increasing effector T cell activity and reducing regulatory T cell (Treg) function. This axis is upregulated in AD skin and blood, highlighting its role in disease pathogenesis.
Area of Science:
- Immunology
- Dermatology
- Molecular Biology
Background:
- Atopic dermatitis (AD) is a chronic inflammatory skin disease.
- Monoclonal antibodies targeting the OX40/OX40L axis show therapeutic potential for AD.
- The precise mechanism of OX40/OX40L in AD pathogenesis remains unclear.
Purpose of the Study:
- To investigate the expression and function of OX40 and OX40L in AD.
- To elucidate the role of the OX40/OX40L axis in T cell activity and inflammation in AD.
Main Methods:
- Skin and blood samples from AD patients and healthy controls (HCs) were analyzed.
- Immunohistochemistry (IHC), immunofluorescence (IF), flow cytometry, RT-qPCR, ELISA, and RNA-seq were employed.
- Purified CD4+ T cells and Tregs were studied.
Main Results:
- Increased OX40 and OX40L expression was observed in AD skin lesions.
- Upregulated OX40 expression on circulating CD4+ T cells and Tregs in AD patients.
- The OX40/OX40L axis maintained Th2 phenotype and decreased IL-10 production by Tregs.
Conclusions:
- AD patients show elevated OX40 expression on effector and regulatory CD4+ T cells.
- The OX40/OX40L axis contributes to skin inflammation in AD.
- This axis impairs Treg function and anti-inflammatory capacity in AD.
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