The immune response to evolving prostate cancer is a complex and carefully orchestrated process. Such a response is initiated when immature dendritic cells take up and process tumor-associated antigens. These dendritic cells must then be activated in order to present peptides to helper (CD4) T cells. Cytolytic (CD8) T cells are next "licensed" to achieve full effector function by interacting with both antigen presenting cells and tumor-specific CD4 T cells. Finally, activated CD8 T cells traffic to sites of neoplasia and mediate killing by multiple mechanisms. This article provides a basic overview of these processes, and discusses the manner by which current clinical interventions seek to augment or initiate an antitumor immune response. Various compensatory mechanisms which serve to down-regulate an antitumor response are also examined.