Immunotherapy response rates in breast cancer remain suboptimal, yet patients with robust T cell infiltration into tumors respond significantly better. Our laboratory investigates how two interconnected barriers limit T cell access to metastatic breast tumors: physical compression of the vasculature by the extracellular matrix, and immunosuppressive signals from cancer-associated fibroblasts (CAFs). We employ strategies to decompress tumor vessels and enhance blood vessel function, thereby promoting T cell infiltration. Simultaneously, we target CAF-produced collagen and other immunosuppressive factors to overcome additional layers of T cell suppression. Our research combines in vivo imaging, adoptive transfer studies, and single-cell transcriptomics to uncover how mechanical decompression combined with strategies targeting CAF-driven immunosuppression can unlock T cell function and improve immunotherapy efficacy in breast cancer.

Recurrent skin infections caused by Staphylococcus aureus drive a devastating cycle of worsening lymphedema through sustained impairment of lymphatic vessel function. Our laboratory investigates how bacterial infection damages lymphatic muscle cells (LMCs)—the contractile cells essential for lymph propulsion and immune surveillance—and how this damage perpetuates chronic lymphatic dysfunction. We characterize the molecular pathways and bacterial factors that impair LMC function, identify novel therapeutic targets through single-cell transcriptomics and functional imaging, and test strategies to restore lymphatic vessel contractility. By elucidating how S. aureus toxins disrupt lymphatic immunity and lymph flow, we aim to develop interventions that preserve lymphatic function, prevent lymphedema progression, and enhance host defense against recurrent infections.