Cellular senescence is a programmed stress response in which cells secrete immunogenic factors that promote senescent cell removal by the immune system or immune surveillance.Different types of senescence occur in pancreatic islet β-cells and senescent β-cells accumulate during aging and diabetes but whether these cells are subject to immune surveillance is unknown.We hypothesize that the subpopulation of stressed senescent β-cells is under immune surveillance to limit their accumulation during aging.Available evidence supports the existence of mechanisms for islet-resident immune surveillance of stressed senescent β-cells involving macrophages and the likelihood of impairment of these mechanisms in diabetes.Elucidation of the mechanisms of islet immune surveillance holds promise for improved therapeutic targeting of senescent β-cells in diabetes. Cellular senescence is a programmed state of cell cycle arrest that involves a complex immunogenic secretome, eliciting immune surveillance and senescent cell clearance. Recent work has shown that a subpopulation of pancreatic β-cells becomes senescent in the context of diabetes; however, it is not known whether these cells are normally subject to immune surveillance. In this opinion article, we advance the hypothesis that immune surveillance of β-cells undergoing a senescence stress response normally limits their accumulation during aging and that the breakdown of these mechanisms is a driver of senescent β-cell accumulation in diabetes. Elucidation and therapeutic activation of immune surveillance mechanisms in the pancreas holds promise for the improvement of approaches to target stressed senescent β-cells in the treatment of diabetes. Cellular senescence is a programmed state of cell cycle arrest that involves a complex immunogenic secretome, eliciting immune surveillance and senescent cell clearance. Recent work has shown that a subpopulation of pancreatic β-cells becomes senescent in the context of diabetes; however, it is not known whether these cells are normally subject to immune surveillance. In this opinion article, we advance the hypothesis that immune surveillance of β-cells undergoing a senescence stress response normally limits their accumulation during aging and that the breakdown of these mechanisms is a driver of senescent β-cell accumulation in diabetes. Elucidation and therapeutic activation of immune surveillance mechanisms in the pancreas holds promise for the improvement of approaches to target stressed senescent β-cells in the treatment of diabetes.