Scientific focus and profile:

Autoimmunity is caused by immune cells attacking harmless self-antigens (or commensal microbes) in host tissues, which they are supposed to protect. Conversely, cancer is a disease in which altered self-cells are not efficiently cleared from the tissue and are thus allowed to multiply. As a target tissue, we study the skin, a crucial barrier of the body against pathogenic invaders that is rich in immune cells. The principal goal of our research is to understand the role of cutaneous T cells and their cross-talk with skin structural cells in autoimmunity, wound healing and cancer. We utilize organotypic 3D-skin cultures and unique (humanized) mouse models to answer our basic research questions and perform preclinical studies. The overall goal of our group is to understand basic mechanisms of tissue immune regulation with the goal to lay the groundwork for novel therapeutic strategies to treat chronic and debilitating inflammatory skin conditions and skin cancer.

Research Network:

Within the International PhD program Immunity in Cancer and Allergy ( and the FWF- funded  SFB-F70 program (awarded by the FWF in 2019) we study the generation of peripheral regulatory T cells in response to skin antigens with a focus on the role of TCR signals and HDACs. In our (pre-)clinical work we collaborate with the  EB house Austria, a Centre of Expertise for Epidermolysis Bullosa (EB) and Special Clinic for “Butterfly Children”. These are a group of patients that suffer from a rare genetic condition in which the skin blisters very easily. In this work, we analyze the immunological consequences of gene therapy of EB patient’s skin, and we also study the role of skin-tropic T cells in the regulation of skin wound healing and cancer development, which aligns well with our role within the  Cancer Cluster Salzburg.

This research group is member of the   Allergy-Cancer-BioNano Research Centre of the University of Salzburg and the  Cancer Cluster Salzburg; the international  “PhD Program ICA” from the FWF and the  SFB-F70 HDACs as regulators of T cell-mediated immunity in health and disease (HIT).