ИСТИНА

Earlier we have found that subendothelial intimacytes in grossly normal human aorta express HLA-DR and CD1a molecules that are involved in peptide and lipid/carbohydrate antigen presentation, respectively. We hypothesize that low density lipoprotein (LDL) stimulates antigen-presenting function in subendothelial cells. To investigate LDL distribution in grossly normal subendothelial intima antibodies against apoB were used. Antigen was visualized using confocal laser scan microscopy and immunohistochemical methods. We localized apoB both inside the cells and associates with extracellular matrix. Intracellular apoB was found both in CD1a and HLA-DR cells. CD1a and HLA-DR were expressed not only by typical antigen-presenting monocyte-derived cells but also by resident intimacytes (peryicytes and smooth muscle cells). HLA-DR and CD1a molecules were associated with membrane antigen-presenting structures and intracellular structures transporting antigen from endoplasmic reticulum to cell surface through antigen-loading vesicles. The size of HLA-DR and CD1a vesicles were similar and ranged from 0.2 to 1
m. Intracellular apoB was colocalized with CD1a vesicles. In HLA-DR cells, the majority of vesicles containing apoB were closely associated with HLA-DR structures but not colocalized. This suggests the difference in antigen processing occurring in HLA-DR and CD1a compartments. CD1aapoB cells were found in association with lymphocytes of various stages of differentiation that may reflect the lymphocyte activation in subendothelial intima. High degree of colocalization of antigenpresenting molecules and apoB supports the suggestion that LDL accumulation in subendothelial intima stimulates activation and differentiation of intimal antigen-presenting cells.