Complement in renal transplantation.
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.
Chowdhury
P
P
Department of Nephrology and Transplantation, Guy's Hospital, King's College, University of London, London, UK.
Zhou
W
W
Sacks
S H
SH
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*
D003181:Complement C4; D010446:Peptide Fragments; D015935:Complement C4b; C032261:complement C4d; D003165:Complement System Proteins