Figure 1.

Immune and inflammatory cells in atherosclerosis. Atherosclerotic lesion (foreground, bottom) and relatively unaffected areas. The endothelial cells above the lesion are polygonal in shape (cobblestone), whereas normal endothelial cells are aligned with the direction of flow. The normal intima is so thin as to be invisible at this level of resolution, but it is greatly expanded in the lesion area, where it contains vascular dendritic cells, macrophages, and foam cells (blue) as well as occasional T lymphocytes (gray). The foam cells surround the necrotic core (brown), which is thought to be composed of foam cells that have undergone secondary necrosis. The normal media is populated by smooth muscle cells that are organized by several elastic laminae (magenta lines). These laminae move apart as the smooth muscle cells assume a secretory phenotype and may form foam cells. Myeloid cells (blue) invade the media in the lesion area. The normal adventitia is populated by sparse T cells (gray), B cells (green), and other lymphocytes (brown) as well as vascular DCs (blue). In the lesion area (bottom), the lymphocytes organize into tertiary lymphoid structures, containing high endothelial venules and other vessels. The angiogenic process eventually leads to neovessels invading the intima, a process that is thought to destabilize plaque and precipitate rupture events. The normal adventitia contains some microvessels (vasa vasorum, in background) that do not penetrate the elastic lamina separating the media from the adventitia.