We are investigating the effects of age, genetics, gender and race on the immune system and on treatment responses in patients with skin disease. We have generated novel bioinformatics approaches to study disease processes in the skin and to establish the determinants of inter-individual heterogeneity, including cross-species analytics, analyses of lncRNA expression in skin and identification of skin specific lncRNA species and use of cytokine and cell-specific expression signatures.

Our group has assigned biologic function to many of the risk variants identified by previous psoriasis genetic studies. Our studies have described the mechanisms by which IFN-γ supports and promotes Th17 responses and have helped identify the function and role of the IL-36 family in cutaneous biology. We have also shown that risk variants influence the direction of inflammation in skin and may drive the variability in treatment responses seen in patients with psoriasis.

We have identified a female-biased molecular switch that heightens immune responses, with current studies seeking to identify epigenetic modifications that drive sexually dimorphic immune responses in keratinocytes. This research aims to accelerate the development of precision therapies for inflammatory skin disorders.