title: Antibody-mediated organ-allograft rejection.
abstract: Recent studies show that alloantibodies mediate a substantial proportion of graft-rejection episodes, contributing to both early and late graft loss. Rejection that is caused by antibody is mediated by different mechanisms from rejection that is caused by T cells, thereby requiring other approaches to treatment and prevention. Antibody induces rejection acutely through the fixation of complement, resulting in tissue injury and coagulation. In addition, complement activation recruits macrophages and neutrophils, causing additional endothelial injury. Antibody and complement also induce gene expression by endothelial cells, which is thought to remodel arteries and basement membranes, leading to fixed and irreversible anatomical lesions that permanently compromise graft function.
authors.affiliation: Department of Pathology, Warren 225, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02140, USA. colvin@helix.mgh.harvard.edu
authors.forename: Robert B
authors.initials: RB
authors.lastname: Colvin
authors.forename: R Neal
authors.initials: RN
authors.lastname: Smith
mesh_terms: D000818:Animals; D003165:Complement System Proteins / Q000276:immunology; D042783:Endothelial Cells / Q000276:immunology; D006084:Graft Rejection / Q000276:immunology*; D006801:Humans; D007518:Isoantibodies / Q000276:immunology*; D014184:Transplantation, Homologous / Q000276:immunology*
chemical_list: D007518:Isoantibodies; D003165:Complement System Proteins