Kraaijeveld R, et al. - This study aimed to investigate the working mechanism behind the possible higher chance of rejection associated with belatacept-induced blockade of the CD80/86-CD28 pathway in kidney transplant recipients, compared with standard, calcineurin inhibitor (CNI)-based therapy. A less proliferative but more cytotoxic profile was displayed by alloantigen activated CD4⁺CD57⁺PD-1^- T-cells as compared with their CD57^- counterparts. Notably, belatacept could partly inhibit their cytotoxic capacity, which did not show any association with the development of rejection after kidney transplantation.