Antigen-Induced Immunomodulation in the Pathogenesis of Atherosclerosis
Figure 2
Morphological features of advanced
atherosclerotic plaques. (a) and (b) show sections from a human carotid
artery; (c) and (d) are sections from an apoE deficient mouse brachiocephalic artery.
Sections (a) and (c) have been stained with haematoxylin and eosin and sections (b) and (d) with van Gieson staining (used to demonstrate the increase of
collagen deposition and development of elastic fibres, a characteristic feature
of the atherogenic process. A positive staining is depicted by a brown colour). L: lumen of the vessel; SR: shoulder region (it is believed to
contain large numbers of proinflammatory cells including macrophages and
lymphocytes, and it is the site related with the onset of the development of
the atherosclerotic plaque); FC: fibrous cap (It also contains large
numbers of mononuclear infiltrate and smooth muscle cells that have migrated
from the media layer (M) and proliferated in response to the
local inflammatory stimuli. It is also characterised by high collagen
deposition and little or no endothelial cells); LC: lipid core (it contains mainly macrophage and smooth muscle
cell-derived foam cells, apoptotic cells, and cholesterol crystals. Older
lesions may also display signs of calcification). Contrasting differences can
be recognised in the anatomic development of atherosclerotic plaques between
human and mouse including the hypertrophy associated with the proliferation of
the smooth muscle cells in the media layer and the fibrous cap. In humans, some
lesions may also contain signs of intraplaque haemorrhage. Signs of plaque
rupture are usually best recognised in mouse (reviewed in [13, 14]).
