Since T-cell-mediated rejection of kidney transplants is now largely preventable or treatable, antibody-mediated rejection (AMR) has emerged as the leading and intractable cause of chronic graft dysfunction and loss. Kidney transplant recipients who develop de-novo donor-specific antibodies have a relative risk of 9·7 for acute AMR and 6·8 for chronic AMR.1–3 Non-specific targeting of B cells, plasma cells, or circulating antibodies is an unsatisfactory strategy for controlling chronic AMR, so alternatives to CD20-specific antibodies (rituximab), intravenous immunoglobulin, proteasome inhibitors (bortezomib), and antibody removal by plasma exchange are clearly needed.
Original Article: [Comment] Immunological investigations empower transplant drug trials