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.
Wasowska
Barbara A
BA
Department of Pathology, The Johns Hopkins University School of Medicine, Ross Bldg. 664B, Baltimore, MD 21205, USA. bwasowsk@jhmi.edu
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