CD40-CD40L interactions in atherosclerosis.
Increasing evidence supports a central role for CD40-CD40L interactions in the pathogenesis of atherosclerosis. Recently, we have shown that CD40L deficiency as well as pharmacological inhibition of CD40L in ApoE(-/-) mice results in the development of a stable atherosclerotic plaque phenotype. This phenotype is rich in smooth muscle cells and collagen, and contains only a small amount of macrophages and T-lymphocytes. CD40 and CD40L protein are present in almost all cell types in human atherosclerotic lesions. Expression was observed in early plaques, but was more predominant in advanced, rupture-prone, and ruptured plaques. Because most of the acute complications of atherosclerosis are the result of plaque rupture, CD40L inhibition might be a novel therapeutic approach to prevent atherosclerotic plaque destabilization and plaque rupture.
Lutgens
Esther
E
Department of Pathology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht, The Netherlands.
Daemen
Mat J A P
MJ
D000818:Animals; D001161:Arteriosclerosis / Q000209:etiology* / Q000517:prevention & control; D019013:CD40 Antigens / Q000502:physiology*; D023201:CD40 Ligand / Q000502:physiology*; D005544:Forecasting; D006801:Humans; D016377:Organ Transplantation / Q000009:adverse effects
D019013:CD40 Antigens; D023201:CD40 Ligand