The laboratory has two principal areas of research focused on understanding i) the pathogenesis of cutaneous autoimmunity and ii) how human pathogens interact with the skin to cause disease.

Most of the studies of cutaneous autoimmunity are utilize samples obtained from patients with autoantibody-mediated autoimmune blistering diseases.  We utilize patient serum to evaluate autoantibody class, subclass, and specificity and measure soluble factors that play a role in immunity. We utilize skin biopsies to measure the direct effects of autoantibodies on skin integrity and determine how the skin-resident immune cell populations are altered in patients with disease compared healthy individuals. Using this approach, we can determine how the autoimmune response evolves over time, resolve disease endotypes, and identify critical cells or factors in disease pathogenesis. By sampling patients longitudinally, at distinct phases of disease through remission, we can identify factors that play a role in the loss of peripheral tolerance in the skin.  Additionally, since the events leading to disease cannot be studied in humans, we are currently working to develop an active mouse model to facilitate studies aimed at understanding the factors that lead to the breakage of immunotolerance and disease onset.

In several collaborative projects, my laboratory aims to determine how the skin cells (immune cells and keratinocytes) participate in diseases caused or exacerbated by pathogens, such as bacteria, viruses and parasites.  Using a variety of in vitro and in vivo infection models, we identify infected cell subsets and define functional changes that contribute to pathogenesis. Most of these studies are aimed at identifying cells or molecules that can be tested as therapeutic targets for prevention or resolution of disease.