Mechanisms controlling myeloid cell mobilization and clearance (i–iii), as well as mechanisms regulating proliferation of myeloid progenitor cells and means of therapeutic intervention (iv–vi), are shown. (i) Levels of plasma CCL2 and CXCL1 critically determine mobilization of myeloid cells from the bone marrow pool into the circulation, whereas CXCL12 exerts retention signals. (ii) Bone marrow CXCL12 levels control homing of senescent myeloid cells to the bone marrow. (iii) Clearance of apoptotic cells by macrophages in peripheral tissue, e.g., in atherosclerotic lesions, unleashes a negative feedback loop involving IL-23 and IL-17. (iv) CCL3 and CXCL8 exert myelosuppressive effects, which are counteracted by CXCL1. (v) Endogenous ApoE bound to proteoglycans interacts with ABCA1 and ABCG1 to enhance cholesterol transportation mechanisms, thereby reducing proliferation of myeloid progenitor cells. (vi) Treatment with LXR agonists enhances expression of ApoE, ABCA1, and ABCG1, thus stimulating cholesterol efflux and dampening proliferation of myeloid progenitor cells. Similarly, cholesterol-poor phospholipid/ApoA-I complexes (rHDL) inhibit proliferation of myeloid progenitor cells. Mechanisms contributing to reduced circulating myeloid cell numbers are shown in red; mechanisms contributing to increased circulating myeloid cell numbers are shown in green; migration or differentiation pathways are shown in black.