Recent data suggest that atherosclerosis might be a systemic (auto)immune r
eaction against heat shock protein 60, first occurring at notorious local p
redilection sites, i.e. the intima at arterial branching points. The local
infiltration of mononuclear cells, mainly macrophage-derived foam cells, T
cells and smooth-muscle cells in atheromatous plaques, have long been descr
ibed. During the past few years, research has been concentrated on the earl
y stages in the development of atherosclerosis, and on healthy arteries fro
m young individuals unaffected by arterial disease. In this review, we summ
arize data characterizing pre-existing mononuclear cell infiltrations in he
althy arteries from children and teenagers. These arterial accumulations at
regions known to be predilection sites for the later development of athero
sclerosis consist mostly of activated T cells, macrophages and dendritic ce
lls, with only a few mast cells and virtually no B or natural killer cells.
In analogy to the mucosa-associated lymphoid tissue, we termed these accum
ulations 'vascular-associated lymphoid tissue', and assumed a similar funct
ion as a local immunosurveillance system, monitoring the bloodstream for po
tentially harmful endogenous or exogenous antigens. In addition to the rema
rkable accumulation of mononuclear cells, the vascular-associated lymphoid
tissue regions are characterized by a typical distribution of extracellular
matrix proteins: collagen type I, collagen type III, fibronectin and tenas
cin are expressed preferentially in the vascular-associated lymphoid tissue
region, whereas collagen type IV, collagen type IV, collagen type VI and l
aminin show a homogenous distribution throughout all regions of the intima.
Vascular adhesion molecules type 1, intercellular adhesion molecules type
1 and P-selectin are already present on the healthy endothelial cells of yo
ung children. Interactions between adhesion molecules, extracellular matrix
components and cellular elements of the vascular-associated lymphoid tissu
e may provide the basis for the cellular accumulations in the vascular-asso
ciated lymphoid tissue regions and the possible development of atherosclero
tic lesions later in life. Curr Opin Lipidol 12:547-553. (C) 2001 Lippincot
t Williams & Wilkins.