What we investigate
Our laboratory investigates the innate and adaptive immune pathways that contribute to inflammatory skin diseases, with a particular focus on lichen planus. Moreover, we are interested in drug-induced skin inflammation. The goal of our research is to open up new relevant research avenues and to identify new therapeutic targets in difficult-to-treat diseases.
KEYWORDS
adverse cutaneous drug reactions, cancer-drug induced skin reactions, innate and adaptive immunity, lichenoid skin inflammation
Our research in more detail
Inflammatory skin diseases are frequent in number and often lead to a decreased quality of life in the affected patients. Lichenoid inflammation is one of the most commonly encountered inflammation patterns of the skin. The prototypical lichenoid mucocutaneous disease is Lichen planus (LP) with its several subtype. Besides, lichenoid inflammation can also be caused by several drugs, in particular cancer drugs such as checkpoint inhibitors, leading to artificial lichenoid skin reactions (ALSR). The exact pathophysiology of both LP and ALSR remains poorly understood.
Our laboratory has identified distinct gene expression patterns between different forms of LP and ALSR, emphasizing the need for a comprehensive investigation into their molecular pathways. We aim to thoroughly characterize the various forms of LP and ALSR and uncover the underlying molecular mechanisms. Ultimately, our goal is to identify key molecules that can serve as targets for developing effective therapies for these challenging skin conditions.
Selected publications
SKINTEGRITY.CH Principal Investigators are in bold:
- Knoch C, Baghin V, Winkelbeiner N, Turko P, Stäger R, Wei K, Banzola I, Mellett M, Levesque MP, Kündig T, French LE, Heinzerling L, Meier-Schiesser B (2024). Distinct variations in gene expression and cell composition across Lichen Planus subtypes. Int J Mol Sci, 25(17), 9720.
- Hess J, Barysch-Bonderer MJ, Seeli C, Laube J, Ghosh A, Deinsberger J, Weber B, Hafner J, Meier-Schiesser B (2024). Identifying key drivers in the pathogenesis of martorell hypertensive ischaemic leg ulcer: a comparative analysis with chronic venous leg ulcer. Acta Derm Venereol, 104, adv40090.
- Hassel JC, Stanhope S, Greenshields-Watson A, Machiraju D, Enk A, Holland C, Abdullah SE, Orloff M, Nathan P, Piperno-Neumann S, Staeger R, Dummer R, Meier-Schiesser B (2024). Tebentafusp induces a T cell driven rash in melanocyte-bearing skin as an adverse event consistent with the mechanism of action. J Invest Dermatol, S0022-202X(24), 01886-4.
- Meier-Schiesser B, Zecha C, S Zierold S, Kolm I, Röckel M, Fröhlich W, Mittag N, Schmitt C, Kumbrink J, Hassel JC, Berking C, Nashan D, French LE, Vera-González J, Dummer R, Kerl-French K, Heinzerling L (2024). Checkpoint inhibitor-induced lichen planus differs from spontaneous lichen planus on the clinical, histological and gene expression level. JAAD Int, 15, 157-164.
- Kraehenbuehl L, Schneider S, Pawlik L, Mangana J, Cheng P, Dummer R, Meier-Schiesser B (2023). Cutaneous adverse events to systemic melanoma treatments: a retrospective single-center analysis. Pharmaceuticals, 16(7), 935.
- Meier-Schiesser B, Feldmeyer L, Jankovic D, Mellett M, Satoh TK, Yerly D, Navarini AA, Abe R, Yawalkar N, Chung WH, French LE, Contassot E (2019). Culprit drugs induce specific IL-36 overexpression in Acute Generalized Exanthematous Pustulosis. J Invest Dermatol, 139(4), 848-858.