Our lab studies how immune responses are regulated within injured and infected tissues with an emphasis on diabetes. We work at the intersection of immunology, structural biology, and microbiology to develop novel therapeutics to promote wound healing and immune tolerance. Major current areas of investigation include:
The Tissue Microenvironment and Immune Regulation in Autoimmune Diabetes
We are studying how the extracellular matrix contributes to immune regulation at sites of inflammation. In particular, we focus on the extracellular matrix polymer hyaluronan and its influence on the number and function of regulatory T-cells in autoimmune, Type 1 diabetes (T1D). We have previously reported that the extracellular matrix contributes to the progression of autoimmune insulitis and other autoimmune diseases. Our current efforts are focused on understanding how the inflamed extracellular matrix influences local antigen presentation and cytolytic killing.
In addition to elucidating fundamental mechanisms of immune regulation, we are working on novel strategies that will prevent T1D and other autoimmune diseases by targeting the extracellular matrix.
The Tissue Microenvironment in Diabetic Wound Healing
Chronic wounds, like tissues under autoimmune attack, are associated with an inflamed extracellular matrix that contributes to immune dysregulation and chronic wounds. We use models of diabetic wound healing to study how the extracellular matrix governs wound healing and local immunity at sites of injury and infection.
The Immunology of Diabetic Wound Infections
Pseudomonas aeruginosa is a major pathogen in diabetic wound infections and other settings. The virulence of Pseudomonas aeruginosa is predicated on its ability to form biofilms. These are networks of host and microbial extracellular matrix that promote colonization, antibiotic resistance, and immune evasion. We are studying how biofilm polymers suppress local immune responses in infected wounds. Further, we are developing innovative strategies to treat chronic infections by disrupting microbial biofilms.