They contain low density lipoproteins (LDL) and can be rapidly detected by examining a fatty plaque under a microscope after it is removed from the body.

[12] Macrophages within the atherosclerotic legion area have a decreased ability to migrate, which further promotes plaque formation as they are able to secrete cytokines, chemokines, reactive oxygen species (ROS) and growth factors that stimulate modified lipoprotein uptake and vascular smooth muscle cell (VSMC) proliferation.

[6] In chronic hyperlipidemia, lipoproteins aggregate within the intima of blood vessels and become oxidized by the action of oxygen free radicals generated either by macrophages or endothelial cells.

[15] Foam cells form the fatty streaks of the plaques of atheroma in the tunica intima of arteries.

The occlusion of small vessels results in ischemia, and contributes to stroke and myocardial infarction, two of the leading causes of cardiovascular-related death.

[16] Foam cells are very small in size and can only be truly detected by examining a fatty plaque under a microscope after it is removed from the body, or more specifically from the heart.

PDCs contribute to the early stages of the formation of atherosclerotic lesions in the blood vessels by releasing large quantities of type 1 interferons (INF).

However, during later stages of lesion progression, pDCs have been shown to have a protective effect by activating T cells and Treg function; leading to disease suppression.

[17] Foam cell degradation or more specifically the breakdown of esterified cholesterols, is facilitated by a number of efflux receptors and pathways.

[2][6][18] Foamy macrophages are also found in diseases caused by pathogens that persist in the body, such as Chlamydia, Toxoplasma, or Mycobacterium tuberculosis.

[20] Lipid-laden alveolar macrophages, also known as pulmonary foam cells, are seen in bronchoalveolar lavage specimens in some respiratory diseases.