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Updated: Jul 6, 2025
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Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
Published on: September 26, 2013
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IL-17A-driven psoriasis is critically dependent on IL-36 signaling
Berenice Fischer1, Tanja Kübelbeck1, Antonia Kolb1
1Department of Dermatology, University Medical Center of the Johannes Gutenberg-University of Mainz, Mainz, Germany.
Frontiers in Immunology
|January 1, 2024
Summary
Targeting the IL-36 receptor (IL36R) pathway with antibodies effectively suppressed skin inflammation in psoriasis models. This approach may offer a new treatment for IL-17A-driven psoriasis and related conditions.
Area of Science:
- Immunodermatology
- Autoimmune diseases
- Molecular biology
Background:
- Plaque psoriasis is a common inflammatory skin condition characterized by keratinocyte hyperproliferation and immune cell infiltration.
- Elevated levels of IL-36 family cytokines are implicated in the pathogenesis of psoriatic skin lesions.
- Anti-IL36 receptor (IL36R) antibodies are approved for generalized pustular psoriasis (GPP), but their efficacy in plaque psoriasis is not fully understood.
Purpose of the Study:
- To investigate the therapeutic potential of IL36R inhibition in plaque psoriasis.
- To evaluate the effects of anti-IL36R antibodies on psoriasis-like skin inflammation and systemic inflammation.
Main Methods:
- Antibody-mediated inhibition of IL36R in imiquimod-induced psoriasis-like skin inflammation models.
- Assessment of disease development in a model dependent on IL-17A overexpression.
- Evaluation of effects on skin and systemic inflammation.
Main Results:
- Antibody-mediated IL36R inhibition suppressed imiquimod-induced psoriasis-like skin inflammation.
- IL36R blockade repressed disease development in an IL-17A-dependent model.
- Treatment with anti-IL36R antibodies reduced both skin and systemic inflammation associated with psoriasis.
Conclusions:
- Inhibition of the IL-36 signaling pathway is effective in suppressing psoriasis-like skin inflammation.
- IL36R blockade may impact keratinocyte and immune cell activation, leading to widespread anti-inflammatory effects.
- Targeting the IL-36 pathway presents a promising alternative therapeutic strategy for IL-17A-driven psoriasis and associated comorbidities.
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