The Gudjonsson Lab is investigating the immunological basis of autoimmune diseases and how genetic risk factors shape the inflammatory network in skin. A primary goal of our work is to establish a foundation of knowledge to support a personalized medicine approach for the treatment of autoimmune disorders, such as psoriasis, psoriatic arthritis, lupus, etc.. Using multi-omics approaches, we are investigating the effects of age, genetics, gender and race on the immune system, and on the course and treatment responses in our patients.
Our scientists have generated bioinformatic approaches to study disease processes in the skin, including novel approaches to establish determinants of inter-individual heterogeneity, 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. These have provided insights and contributed to our understanding of human skin diseases.
Our group has assigned biologic function to many of the risk variants identified by previous psoriasis genetic studies. We 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. Our work has 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.
In addition, we have identified a female biased molecular switch that heightens immune responses. In ongoing work, we seek to identify and target epigenetic modifications that drive sexually dimorphic immune responses in keratinocytes with the aim of supporting future development of precision therapies for inflammatory skin disorders.