CD137 belongs to the tumor necrosis factor receptor group which comprise of cytokines that play a significant role in triggering inflammatory events following an injury in cells. It is generally expressed in activated T cells aside from CD8 T cells and CD4 T cells. An interesting characteristic of CD137 is its co-stimulatory effect at the immune checkpoint, and this is one of the reasons why immunologists have taken strong interest on this molecule. Numerous studies have found that CD137 plays a crucial part in atherosclerosis development. The main goal of this thesis is to explain the function of CD137 in the development of atherosclerosis. It also aims to explain the mechanisms behind the activation of CD137 signaling and expression atherosclerotic lesions as well as investigate the role of CD137 in immune regulation and inflammation. Moreover, the investigation of the function of CD137 in leukocyte migration and cell adhesion as well as the association between CD137 and plaque stability were taken into consideration in the thesis. Finally, it aims to explain the relationship between CD137 and the clinical events of cardiovascular diseases. In human immune cells, the expression of CD137 results to the development of plaque inflammation, which advances to atherosclerotic plaque. In addition, research findings also suggest that CD137 constitutes a potential factor for the destabilization of plaques and it also promotes higher risk for the occurrence of plaque thrombosis. Further research is suggested with regard to genetic pathways involved with CD137 signaling as well as its participation in tumor therapy and other mechanisms.