The focus of our laboratory is to understand how cutaneous inflammation is induced and to utilize that knowledge to develop novel therapeutics utilizing both murine and human models. In our first project we are examining the role of danger signals, specifically ATP/P2X7R, in the development and maintenance of psoriatic lesions. We have determined that signaling through the P2X7R in vitro leads to the differentiation of Th17 cells, utilizing both human and murine cells. Moreover, if P2X7R agonists are injected into the skin we can induce an acute psoriasis-like response in mice, indicating that ATP/P2X7R likely has a role in initiating the development of psoriasis lesions. In our second project, we have determined that an exemplary electrophilic nitro fatty acid, OA-NO2, has the capacity to suppress contact hypersensitivity responses, we hope to eventually translate this finding into psoriasis models. Furthermore, we are focused on understanding the mechanisms by which OA-NO2 suppresses cutaneous inflammation in order to better understand these inflammatory processes.
To explore pertinent questions of cutaneous biology, over the last several years our laboratory has utilized human skin explants. We have also successfully performed human xenotransplants with biopsies that we have collected from healthy human skin and we are now moving into transplanting psoriatic lesional skin. Additionally, over the last few years we have begun to extend our findings from healthy skin into murine models of psoriasis.