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REGULATION OF LEUCOCYTE‐ENDOTHELIAL INTERACTIONS OF SPECIAL RELEVANCE TO ATHEROGENESIS

1 The cellular events underlying atherosclerosis include the accumulation of lipid‐laden monocytes in the neointima. This process is associated with the expression of adhesion proteins and chemokines by the endothelium, in a manner similar to that seen after the administration of pro‐inflammatory cytokines to endothelial cells. 2 The processes that limit endothelial responses to proinflammatory cytokines are, therefore, the subject of this paper. Evidence is presented that the cytokine TGF‐β exerts a tonic inhibitory influence on endothelial responses. Furthermore, the smooth muscle cells adjacent to endothelial cells have a similar effect to exogenous TGF‐β and this suggests that these two cells form a functional interactive unit. Finally, the atheroprotective lipid fraction, high‐density lipoproteins (HDL), also inhibits endothelial activation. The mechanism of effect of HDL that appears separate from its traditional role in cholesterol transport may yield novel insights into atheroprotection.