However, the pathogenesis of atherosclerosis is still poorly understood. Controversy exists about the participation of innate immunity involving macrophages and natural killer cells vs antigen-specific acquired immunity involving lymphocytes.
Macrophages predominate in atherosclerotic lesions.
Natural killer cells, although a smaller number, are also present. Moreover, T lymphocytes that participate in acquired immunity are often present in lesions and can modulate lesion progression. Using mouse models of hyperlipidemia, we are addressing in vivo the participation of both innate inflammatory responses and acquired immune responses in atherosclerosis. CD43 is a leukocyte cell-surface sialoglycoprotein or mucin that has both antiadhesive and proadhesive properties and may influence entry of leukocytes into atherosclerotic lesions of the vessel wall. Atherosclerosis was allowed to develop for several months.