Our laboratory studies the innate and adaptive immune pathways leading to lichenoid skin reactions including the frequent inflammatory skin disease Lichen planus and drug-induced lichenoid reactions (e.g. by checkpoint inhibition), as well as leading to other severe adverse drug reactions of the skin. The goal of our research is to open up new relevant research avenues and to identify new therapeutic targets in difficult-to-treat diseases.
adverse cutaneous drug reactions, cancer-drug induced skin reactions, innate and adaptive immunity, lichenoid skin inflammation
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 subtypes. Cell-mediated cytotoxicity is regarded as a major pathomechanism of LP, thereby resembling artificial lichenoid skin reactions (ALSR) induced by immune checkpoint inhibitors. However, the exact pathophysiology remains unclear. Our laboratory demonstrated distinct gene expression patterns between the different forms of LP and ALSR, underlining the need of a detailed investigation of molecular pathways of LP and ALSR. We aim to characterize the different forms of LP and ALSR, using integrated transcriptomic profiling with surface proteomics on a single cell level, high-dimensional single-cell analysis using Time of Flight Mass Cytometry, followed by the investigation of the molecular mechanism using state-of-the-art-techniques for gene modification such as CRISPR-Cas9 in three-dimensional skin-equivalent models. The aim of our research is to identify key molecules as targets for future therapies of these difficult-to-treat skin diseases.
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