CD40 co-stimulatory molecule expression by dendritic cells in primary atherosclerotic lesions in carotid arteries and in stenotic saphenous vein coronary artery grafts

Inflammation in Vein Graft Disease

“…Dendritic cells, originating from Ly-6C lo monocytes, are found in all layers of the vein graft and colocalize with T cells as antigen presenting cells ( 148 ). In vein grafts dendritic cells are capable of triggering T cells by costimulation of CD40 ( 149 ).…”

“…It has been shown that T cells are capable of proliferation in vein grafts ( 152 ). Furthermore, interaction between dendritic cells and T cells in a CD40 dependent manner have been observed in vein grafts ( 149 ). However, little is known about the exact function and role of T cells in the pathophysiology of VGD.…”

Dendritic Cells and Their Role in Cardiovascular Diseases: A View on Human Studies

“…Cherian et al investigated the presence of DCs in vein grafts and found DCs positive for S100 and CD1a in the vascular walls of these vessel grafts [ 35 ]. A further study on stenotic vein coronary bypass grafts demonstrated that DCs positive for the costimulatory molecule CD40 were clustered within the intima as well as in the media and adventitia [ 38 ]. In accordance with the results on human coronary bypass grafts, it has been demonstrated that T cells were accumulated in the vascular wall of saphenous vein grafts [ 39 ].…”

Dendritic cells and their role in atherogenesis

“…140 DCs clustering with T cells display the intercellular cell adhesion molecule-1 and VCAM-1, 60 interactions of which with leukocyte function-associated antigen-1 and very late activation antigen-4, respectively, are essential for T-cell activation. 141 In DC/T-cell interactions, DCs display CD40 60,142 and express high levels of HLA-DR 60 and CD1 molecules. 60,73,74 An experimental in vivo study has shown that trafficking of monocyte-derived DCs from atherosclerotic plaques occurs during lesion regression, but little DC emigration has been detected from progressive plaques, suggesting that the progression of atherosclerotic plaques may result not only from www.laboratoryinvestigation.org | Laboratory Investigation | Volume 90 July 2010the robust monocyte recruitment into arterial walls but also from the reduced emigration of DCs from lesions.…”