Monocytes/macrophages, T lymphocytes, and vascular dendritic cells, which are involved in both innate and adaptive immunity, play important roles in the development and progression of atherosclerosis. However, studying atherosclerosis progression in humans is challenging as lesion formation can take several decades and there are many constraints on obtaining human arterial samples. Therefore, numerous animal models have been utilized to study atherosclerosis. Initially, the dynamics of cellular changes in early lesion formation were primarily investigated using rabbit models (see Chap. 20 for details). Subsequently, the development of mouse models with apolipoprotein E (ApoE) or low-density lipoprotein receptor (LDLr) gene deficiency, which are highly susceptible to atherosclerosis, has led to a surge in mouse-based research. The widespread use of genetically engineered (transgenic, knockout, and knock-in) mouse models has enabled the verification of hypotheses and inferences about the initiation and progression of atherosclerosis by targeting specific genes.