Purpose of review: This review relates recent findings that highlight the role of the spleen as an active donor of monocytes during inflammation, with a special focus on atherosclerosis.
Recent findings: The contribution of hypercholesterolemia and monocytes/macrophages to atherosclerotic lesion formation is undisputable. The origin of plaque macrophages is, however, still a subject of debate as to whether they derive from local amplification of (resident) macrophages or from continuous recruitment and differentiation of monocytes. Recently, the spleen has emerged as an important reservoir of monocytes that contributes to lesion growth. The regulation of monocyte mobilization from the splenic compartment has, therefore, raised a keen interest in understanding the cellular and molecular mechanisms involved in this process.
Summary: Impaired regulation of cholesterol metabolism increases the proliferation of hematopoietic stem and progenitor cells in both the bone marrow and the spleen. Recent findings identified the implication of angiotensin II, red pulp macrophages and B-lymphocytes as partners of monocyte expansion in, and mobilization from the spleen. Future studies will help in understanding the mechanisms of monocyte mobilization and its precise roles in atherosclerosis, and whether modulation of the splenic components may become a promising future direction in the prevention and treatment of cardiovascular diseases.