Complement membrane attack complex and protectin (CD59) in liver allografts during acute rejection

Background/Aims: The complement system is important in the rejection of xen ografts, but very little is known about its activation in the rejection of allografts, Complement lysis is induced by the membrane attack complex (MAC ), an aggregate of C5b, C6, C7, C8 and C9 molecules. The main defender agai nst MAC is the CD59 molecule, also called protectin, In this study, the aim was to analyze the possible deposition of MAC and the fate of CD59 on dist inct cell. populations during liver allograft rejection. Methods: Liver allografts were monitored by frequent fine-needle aspiration biopsies (FNAB) to demonstrate the immunoactivation of rejection. To exami ne MAC and CD59 in the FNAB, in relation to the activation markers of rejec tion, IL2-receptor, MHC class II and ICAM-1 expression, specific monoclonal antibodies and immunoperoxidase staining were used. Results: Ten out of 21 consecutive liver transplants underwent a histologic ally confirmed episode of reversible acute rejection. In the FNAB, a signif icant increase of the activation markers IL2-receptor, class II and ICAM-1 correlated with the peak of inflammation during the episode. In association with inflammation, a significant deposition of MAC was recorded in neutrop hils and lymphocytes infiltrating the graft and in the parenchymal cells, M AC deposition subsided together with the inflammation. A significant decrea se in CD59 expression was seen in neutrophils during rejection, but CD59 ex pression on other inflammatory cells and hepatic tissue cells varied greatl y. Conclusions: Complement activation was seen in association with acute rejec tion of liver allografts and it led to MAC assembly on leukocytes and tissu e cells. A decrease in CD59 expression was less clear-cut, but it may predi spose the cells to complement-mediated elimination.