Antibody-Mediated Rejection: the Role of Plasma Cells and Memory B Cells

摘要

Purpose of Review Antibody-mediated rejection (ABMR) is one of the most common causes of renal allograft loss. This review aims to outline the different clinical scenarios of ABMR with an emphasis on the cellular sources of antibody. Recent Findings Studies of human plasma cells (PC) and memory B cells have been limited, but existing data suggest that both can contribute to ABMR. Hyperacute ABMR is due to pre-existing anti-HLA antibodies. Early acute ABMR likely involves the stimulation of memory B cells and can lead to new long-lived plasma cells. Late acute ABMR involves the de novo development of new memory B cells and PCs that are resistant to conventional immunosuppression. Chronic active ABMR involves not only antibodies (either pre-existing or de novo) but also effector cells such as NK cells, T cells, and macrophages. Cellular processes underlying ABMR involve interactions between memory B cells, plasmablasts, plasma cells, and various effectors. Understanding these cellular processes is needed to improve therapies for ABMR.