Myr research focuses on understanding how skin-associated microbes shape immune responses during infection, inflammation, and wound healing. We investigate how interactions among the skin microbiome, epithelial cells, regulatory T cells (Tregs), conventional T cells, and innate lymphocytes determine whether immune responses promote host defense and tissue repair or become dysregulated and lead to chronic inflammation and impaired healing. A major focus of the laboratory is to define how Tregs maintain their stability and suppressive function in the skin, and which microbial, inflammatory, and tissue-derived signals drive Treg instability and functional plasticity across different inflammatory settings. We are particularly interested in how wound-associated microbes, including Staphylococcus aureus and Pseudomonas aeruginosa, as well as commensal bacteria such as Staphylococcus epidermidis, influence these immune programs. By integrating mouse models, human skin and wound samples, cellular systems, and multi-omics approaches, our long-term goal is to identify immune and microbial pathways that can be targeted to control infection, restore immune balance, and improve wound healing.