Since the conceptual proposal of cancer immunosurveillance by Burnet and Smith more than a half-century ago, a recent success of immune checkpoint blockade therapy in human cancers has provided a breakthrough in cancer immunotherapy. PD-1, originally discovered by Dr. Honjo’s group at Kyoto University in 1992, is a TCR-coinhibitory receptor and plays a crucial role in the checkpoint of peripheral T-cell self-tolerance, and in 2002 we reported that the PD-1 checkpoint also takes an important part in restraining endogenous anti-tumor immunity, providing a basis for current immune checkpoint blockade therapy. Current major research is directed to improved efficacy of the therapy as well as the search for genetic and other biomarkers predictive of the effectiveness. The clinical studies have reinforced the crucial importance of general accessibility of host immune effector system to cancer cells in tumor microenvironment. Another important aspect in cancer immunity is the host immune status. Considering the increased risk of cancer emergence with age, age-dependent alteration of immune capacity, or immunosenescence, may have a potential importance in cancer immunity. A recent report demonstrating that selective elimination of senescent cells in tissues lead to prolonged lifespan with decreased spontaneous tumor development may supports the notion. We recently succeeded in identifying senescent-associated (SA-) T cells, which play a central role in the immune senescence phenotype. While defective in proliferation capacity, SA-T cells are metabolically highly active and are involved in a variety of age-related disorders. In this talk, I shall briefly summarize the history and recent advancement in immune checkpoint blockade therapy and also introduce our recent studies on immunosenescence, which may potentially affect cancer immunosurveillance mechanism in hosts.