Mechanisms involved in antibody- and complement-mediated allograft rejection.
Antibody-mediated rejection has become critical clinically because this form of rejection is usually unresponsive to conventional anti-rejection therapy, and therefore, it has been recognized as a major cause of allograft loss. Our group developed experimental animal models of vascularized organ transplantation to study pathogenesis of antibody- and complement-mediated endothelial cell injury leading to graft rejection. In this review, we discuss mechanisms of antibody-mediated graft rejection resulting from activation of complement by C1q- and MBL (mannose-binding lectin)-dependent pathways and interactions with a variety of effector cells, including macrophages and monocytes through Fcgamma receptors and complement receptors.
Department of Pathology, The Johns Hopkins University School of Medicine, Ross Bldg. 664B, Baltimore, MD 21205, USA. bwasowsk@jhmi.edu
Barbara A
BA
Wasowska
D000818:Animals; D003167:Complement Activation / Q000276:immunology*; D004195:Disease Models, Animal; D042783:Endothelial Cells / Q000473:pathology; D006084:Graft Rejection / Q000276:immunology / Q000473:pathology*; D016027:Heart Transplantation / Q000276:immunology; D006801:Humans; D007518:Isoantibodies / Q000276:immunology*; D008264:Macrophages / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D009000:Monocytes / Q000276:immunology
D007518:Isoantibodies