My research program – working as a part of a larger group of researchers in the lab of Akiko Iwasaki, PhD – focuses on the biology of autoimmune inflammatory skin diseases. To accomplish our research, we utilize unique genetic mouse models of autoimmunity, in addition to patient samples from autoimmune skin disease patients who I see in my clinic. While our work is currently focused on lupus erythematosus, we plan to extend our observations to other relevant skin diseases like dermatomyositis that on some levels appear to have shared molecular and cellular biology. To accomplish these studies, we regularly employ a mix of both standard and newer technologies including high parameter flow cytometry, bulk RNA sequencing, single cell RNA sequencing, in addition to spatial transcriptomic analyses:
- Type I interferons and their role in autoimmune skin disease: Type I interferons are the canonical vertebrate anti-viral signaling program and are elevated in autoimmune diseases like systemic lupus erythematosus and dermatomyositis. The receptors for type I interferons are expressed broadly in nearly all cell types, though the inflammation in these diseases is often more restricted to certain organ systems like the skin. We seek to understand the influence of these antiviral programs on specific cell populations in the skin and how they mediate pathology.
- The origins of autoimmune inflammation: Though elevated antiviral signaling is well-established in autoimmune diseases like systemic lupus erythematosus, the origins of these elevations are currently unknown. We are evaluating the role of endogenous retroelements as the proximal cause of the elevated interferon signaling observed in select autoimmune diseases like lupus.