|Education||BS, University of California San Diego|
Programed death 1 (PD-1) and programmed death ligand 1 (PD-L1) have revolutionized the field of immunotherapy in solid tumors. Interaction between PD-1 and PD-L1 reduces T-cell activation and is used as an “immune checkpoint” to restrain T-cell activation under normal conditions. However, many tumors (which can express high levels of PD-L1) can hijack this checkpoint, allowing it to escape immune surveillance. Several solid tumors including melanoma, RCC, NSCLC, breast and ovarian cancer have yielded clinical responses with anti-PD-1 therapy. Of particular interest to our lab is Multiple Myeloma (MM), a lymphoid tumor. Intriguingly, while MM tumor expresses high levels of PD-L1, anti-PD-1 therapy has shown no clinical benefit in MM. My project is focused on determining the role and mechanism of PD-1 and PD-L1 in MM.