ORIGINAL RESEARCH article
Front. Med.
Sec. Dermatology
Volume 12 - 2025 | doi: 10.3389/fmed.2025.1663279
HUMAN EPIDERMIS MODELS DEMONSTRATE MEDIATOR ROLE OF TLR2 AND TLR3 FOR PSORIATIC INFLAMMATION
Provisionally accepted
- Fraunhofer Institute for Interfacial Engineering and Biotechnology, Stuttgart, Germany
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Psoriasis is a multifactorial systemic autoinflammatory disease that is characterized by complex signaling between keratinocytes and immune cells. The trigger factors for the cutaneous manifestation of the disease are divers but have in common that they induce an activation of the Tolllike receptor (TLR) signaling pathways. This is best described for the activation of TLR7/8/9 in dendritic cells. In this study, we investigated the role of TLR2 and TLR3 activation in keratinocytes for the expression of psoriatic hallmarks in the skin. We set up 3D epidermis models using wild type keratinocytes and TLR2 knockout and TLR3 knockout (KO) keratinocytes derived from the wild type keratinocytes and treated them with TLR agonists. Immunohistochemical, Western Blot and multiplex analysis showed that the TLR activation induced the expression of psoriasis associated markers like S100A7, p-STAT3, CXCL-1, IL-8, IL-1α, S100A9 and IL-23 in the wild type but not in the TLR KO epidermis models. Thus, TLR2 and TLR3 activation in keratinocytes individually contributes significantly to induce the release of cytokines and other immune modulators characteristic for a psoriasis like inflammation in 3D epidermis models.
Keywords: Psoriasis, Toll-like receptor, in vitro epidermis model, Keratinocytes, Cytokines
Received: 10 Jul 2025; Accepted: 25 Aug 2025.
Copyright: © 2025 Glasebach, Denzinger, Rupp and Dr. Burger-Kentischer. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Hanna Glasebach, Fraunhofer Institute for Interfacial Engineering and Biotechnology, Stuttgart, Germany
Anke Dr. Burger-Kentischer, Fraunhofer Institute for Interfacial Engineering and Biotechnology, Stuttgart, Germany
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