Immune checkpoint blockade (ICB) has revolutionized the ways in which we treat some cancers, producing durable responses. However, many patients fail to respond to ICB. It is theorized that patients require tumor-specific T cells to respond effectively to ICB, but aged individuals have compromised T cell diversity partially due to reduced thymic output. The goal of this dissertation is to determine the role of a common target of ICB, programmed cell death protein 1 (PD-1), in regulating T cell development in the thymus.