Post-transplant immune activation: innocent bystander or insidious culprit of post-transplant accelerated atherosclerosis.
Fiche publication
Date publication
octobre 2016
Journal
Cell transplantation
Auteurs
Membres identifiés du Cancéropôle Est :
Pr DUCLOUX Didier
Tous les auteurs :
Ducloux D, Bamoulid J, Crepin T, Rebibou JM, Courivaud C, Saas P
Lien Pubmed
Résumé
Cardiovascular disease is a major cause of morbidity, disability, and mortality in kidney transplant patients. Cumulative reports indicate that the excessive risk of cardiovascular events is not entirely explained by the increased prevalence of traditional cardiovascular risk factors. Atherosclerosis is a chronic inflammatory disease and it has been postulated that post-transplant immune disturbances may explain the gap between the predicted and observed risks of cardiovascular events. However, whereas concordant data suggest that innate immunity contributes to the posttransplant accelerated atherosclerosis, only few arguments plead for a role of adaptive immunity. We report and discuss here consistent data demonstrating that CD8(+) T cell activation is a frequent post-transplant immune feature that may have pro-atherogenic effects. Expansion of exhausted/activated CD8(+) T cells in kidney transplant recipients is stimulated by several factors including: cytomegalovirus (CMV) infections, lymphodepletive therapy (e.g., anti-thymocyte globulins), chronic allogeneic stimulation and a past of renal insufficiency. This is observed in the setting of a decreased thymic activity, a process also found in elderly individuals and reflecting accelerated immune senescence.
Référence
Cell Transplant. 2016 10;: