Our lab studies how inflammatory skin diseases are immunologically initiated and sustained. Our studies are driven by observations in patients and carried out on human tissues. Our goal is to gain fundamental insights into the immunobiology of skin disease and apply these findings to develop novel therapies that improve patients’ lives. We focus on two inflammatory skin diseases: vascular composite allograft rejection and autoimmune fibrosis.
Vascular Composite Allograft Rejection
Vascularized composite allografts (VCA), including face and limb transplants, hold great promise for restoring function in patients who have suffered devastating traumatic injuries. BWH was the site of the nation’s first face transplant in 2011. Since that time, there have been 9 face transplant procedures at BWH and over 50 around the world. Recurrent immunologic rejection is the largest barrier to wider implementation of VCA. Our studies have helped identify mechanisms underlying T cell driven VCA rejection. Our ongoing studies seek to identify superficial epidermal biomarkers to improve rejection diagnosis, evaluate the utility of sentinel flaps for remote site rejection monitoring, identify early events that lead to chronic rejection, and identify anti-rejection therapeutic targets.
Fibrotic Connective Tissue Diseases
Fibrosis is a leading cause of mortality worldwide and contributes to the progression of many chronic diseases, including fibrotic skin conditions. Morphea and eosinophilic fasciitis (EF) are autoimmune fibrosing skin diseases that are often grouped under the same clinical umbrella, yet their pathogenesis remains poorly understood. In collaboration with Dr. Avery LaChance, we have identified a role for antigen-activated T cells, immunogenic cell death, innate danger sensors, and JAK/STAT activation as shared mechanisms driving fibrosis in both morphea and EF. Currently, no cure exists for established fibrosis. Our ongoing studies aim to understand how chronic cutaneous fibrotic injury persists, with the goal of identifying therapeutic targets to halt disease progression and potentially reverse established fibrosis.
