Therapeutic Sciences Graduate Program

Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by persistent synovial inflammation and progressive cartilage and bone destruction. Using genetic mouse models and human RA fibroblast-like synoviocytes, our lab has identified SHP2, encoded by PTPN11, as an important regulator of pathogenic synovial signaling and joint destruction. My research investigates the cell-specific roles of SHP2 in FLS and myeloid-lineage cells and evaluates the SHP2-targeting PROTAC, D26 in mouse models of inflammatory arthritis. My goal is to define how genetic and pharmacologic SHP2 depletion regulates inflammation, osteoclastogenesis, and bone erosion and evaluate targeted SHP2 degradation as a therapeutic strategy for RA.