Macrophages possess a number of surface receptors that are capable of mediating the internalization of lipoproteins. The low-density lipoprotein (LDL) receptor of human monocyte macrophages recognizes apolipoprotein B-100 and apolipoprotein E and is rapidly regulated in response to changes in intracellular cholesterol levels. In contrast, in J774 macrophages LDL receptor regulation is defective and LDL can cause massive cholesterol accumulation. The β migrating very low density lipoprotein (β-VLDL) receptor is poorly regulated by cellular cholesterol concentrations, readily recognizes apolipoprotein E, poorly recognizes apolipoprotein B-100, and is immunologically related to the LDL receptor. The scavenger receptor (acetyl-LDL receptor) appears to have a molecular weight of 250 000 and is not regulated by cellular cholesterol levels. This receptor recognizes LDL that has been chemically or biologically altered. LDL complexes can also enter macrophages and cause cholesterol accumulation. Examples of such complexes are LDL–dextran sulphate complexes, LDL–proteoglycan aggregates, LDL–mast cell granule complexes, LDL–heparin–fibronectin–denatured collagen complexes, and LDL–antibody complexes. The entry of lipoprotein into macrophages by a pathway that is poorly regulated or is not regulated by cellular cholesterol concentrations appears to be a prerequisite for the formation of arterial foam cells.

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