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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 trialsNEXT ARTICLE
An antibody is a protein produced by the body's immune system when it detects harmful substances, called antigens. Examples of antigens include microorganisms (such as bacteria, fungi, parasites, and viruses) and chemicals. Antibodies may be produc...