title: Complement in renal transplantation.
abstract: Previous research and therapy in renal transplantation largely focused on the cellular arm of the adaptive immune response. Evidence is emerging that innate immune mechanisms, particularly complement, play a greater role in inflammatory and immune responses against the graft than has been previously recognized. Alternative complement pathway activation appears to mediate renal ischaemia/reperfusion injury, and proximal tubular cells may be both the source and the site of attack of complement components in this setting. Locally produced complement also plays a role in the development of both cellular and antibody-mediated immune responses against the graft. C4d staining has emerged as a useful marker of humoral rejection both in the acute and in the chronic setting and led to renewed interest in the significance of anti-donor antibody formation. A number of therapies are in development which inhibit complement or reduce local synthesis, and may lead to an improved clinical outcome following renal transplantation.
authors.affiliation: Department of Nephrology and Transplantation, Guy's Hospital, King's College, University of London, London, UK.
authors.forename: P
authors.initials: P
authors.lastname: Chowdhury
authors.forename: W
authors.initials: W
authors.lastname: Zhou
authors.forename: S H
authors.initials: SH
authors.lastname: Sacks
mesh_terms: D003181:Complement C4 / Q000378:metabolism; D015935:Complement C4b; D003165:Complement System Proteins / Q000378:metabolism*; D006084:Graft Rejection / Q000378:metabolism*; D006801:Humans; D016030:Kidney Transplantation; D010446:Peptide Fragments / Q000378:metabolism; D015427:Reperfusion Injury / Q000378:metabolism*
chemical_list: D003181:Complement C4; D010446:Peptide Fragments; D015935:Complement C4b; C032261:complement C4d; D003165:Complement System Proteins