CHIP arises from somatic mutations in hematopoietic stem cells that yield mutant clonal progeny in the blood. CHIP frequency increases with age and has coincidentally emerged as an independent and strong risk factor for atherosclerotic disease. However, species-specific differences limit direct translation from mouse models to humans. We aim to generate a novel atherosclerotic mouse model harboring a humanized immune system with clonal hematopoiesis, allowing the study of mutant human leukocytes and inflammatory mediators in atherosclerotic plaque development. We expect that this will provide a unique opportunity to assess the contribution of human immune cells to vascular health, provide new insights into basic human vascular biology, and enable the study of a broad spectrum of clinically relevant vascular diseases.
