Our research focuses on the understanding of mechanisms that initiate and maintain inflammation in the skin. Amongst others, one of those mechanisms involves dermal infiltration by plasmacytoid dendritic cells and their activation to produce type I interferons.
plasmacytoid dendritic cells (pDCs), psoriasis, skin inflammation, tumor microenvironment, venereology
Understanding cellular and molecular pathways involved in inflammation of the skin is the focus of our research. For dermal infiltration by pDCs, as mentioned above, we identified a new inflammatory pathway. We also found that this pathway is over-activated in psoriasis and lupus, where it drives chronic inflammation and disease initiation. This pathway is activated in injured skin, but it is self-limited, providing a well-controlled initial inflammatory stimulus that promotes the wound healing response.
More recently, we found that this inflammatory pathway is also at the heart of a side effect of anti-TNF treatment, called paradoxical psoriasis. In contrast to psoriasis, paradoxical psoriasis is characterized by an exaggerated activation of skin pDCs that does not lead to T cell autoimmunity. The delicate balance between TNF and type I IFN signalling can be disturbed by anti-TNF treatment, leading to paradoxical psoriasis as a side-effect of the treatment. These findings provides a basis for the design of new strategies targeting pDCs and type I IFN for the treatment and prevention of paradoxical psoriasis.
With this and other research projects, we contribute to SKINTEGRITY.CH with the aim to improve the mechanistic understanding of skin inflammation as well as its treatment in the clinic.
SKINTEGRITY.CH Principal Investigators are in bold: