Alicia R. Mathers Ph.D.

Understanding induction of cutaneous inflammation, in particular psoriasis and wound healing; 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, nitro oleic 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, our laboratory has utilized human skin explants and murine models of disease. We also perform human to mouse skin xenotransplants with biopsies that we have collected from healthy human skin and (non)psoriatic lesional skin. The Mathers lab has two R01 funded projects (2016-2020) to study cutaneous inflammation and psoriasis. Graduate students interested in rotation opportunities should contact Dr. Mathers.