Complement in organ transplantation

被引:45
作者
Asgari, Elham [1 ]
Zhou, Wuding [1 ]
Sacks, Steven [1 ]
机构
[1] Kings Coll London, MRC, Ctr Transplantat, Guys Hosp, London SE1 9RT, England
基金
英国惠康基金;
关键词
complement; rejection; transplantation; RENAL-ALLOGRAFT REJECTION; ANTIBODY-MEDIATED REJECTION; DELAYED GRAFT FUNCTION; T-CELLS; DENDRITIC CELLS; SURVIVAL; DONOR; C5A; DEFICIENCY; ACTIVATION;
D O I
10.1097/MOT.0b013e32833b9cb7
中图分类号
R3 [基础医学]; R4 [临床医学];
学科分类号
1001 ; 1002 ; 100602 ;
摘要
Purpose of review The aim of this review is to bring to attention the most recent advances made in understanding the role of complement components in both innate and adaptive immune responses in solid organ transplantation with emphasis on the kidney. Recent findings Alongside recent findings related to the role of anaphylatoxins in modulating adaptive immune responses, there has been a genomic study to assess the expression of inflammatory markers in kidney transplantation, showing significant involvement of some complement molecules in predicting graft function. Modulators of complement pathway activity such as decay accelerating factor (CD55) and CD59 have also been shown to have a role in graft rejection. Potential new therapeutic targets related to complement proteins are being investigated. Summary The mechanism of rejection in solid organ transplantation is influenced by the initial inflammatory response and subsequent adaptive allo-immune response, both of which have been shown to be affected by various complement components. Due to limitations of existing treatments, new approaches are needed to better control these responses to improve graft survival. Built on an expanding knowledge of complement involvement, targeted blocking of the effector complement molecules and modulating the expression of complement inhibitors has suggested potentially useful approaches for reducing the effect of inflammatory damage from cold ischaemia as well as reducing the activation of the adaptive immune system related to complement.
引用
收藏
页码:486 / 491
页数:6
相关论文
共 39 条
[1]   C1q enhances IFN-γ production by antigen-specific T cells via the CD40 costimulatory pathway on dendritic cells [J].
Baruah, Paramita ;
Dumitriu, Ingrid E. ;
Malik, Talat H. ;
Cook, H. Terence ;
Dyson, Julian ;
Scott, Diane ;
Simpson, Elizabeth ;
Botto, Marina .
BLOOD, 2009, 113 (15) :3485-3493
[2]   Prospects and limitations of post-transplantation alloantibody detection in renal transplantation [J].
Boehmig, Georg A. ;
Bartel, Gregor ;
Regele, Heinz ;
Wahrmann, Markus .
HUMAN IMMUNOLOGY, 2009, 70 (08) :640-644
[3]   Expression of the Decay-Accelerating Factor (CD55) in Renal Transplants-A Possible Prediction Marker of Allograft Survival [J].
Brodsky, Sergey V. ;
Nadasdy, Gyongyi M. ;
Pelletier, Ronald ;
Satoskar, Anjali ;
Birmingham, Daniel J. ;
Hadley, Gregg A. ;
Obeidat, Khaled ;
Nadasdy, Tibor .
TRANSPLANTATION, 2009, 88 (04) :457-464
[4]   Antibody-mediated renal allograft rejection: Diagnosis and pathogenesis [J].
Colvin, Robert B. .
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, 2007, 18 (04) :1046-1056
[5]  
CORNELL LD, AM TRANSPL C 2009
[6]   Complement protein C1q induces maturation of human dendritic cells [J].
Csomor, Eszter ;
Bajtay, Zsuzsa ;
Sandor, Noemi ;
Kristof, Katalin ;
Arlaud, Gerard J. ;
Thiel, Steffen ;
Erdei, Anna .
MOLECULAR IMMUNOLOGY, 2007, 44 (13) :3389-3397
[7]   Complement and renal transplantation: From donor to recipient [J].
Damman, Jeffrey ;
Schuurs, Theo A. ;
Ploeg, Rutger J. ;
Seelen, Marc A. .
TRANSPLANTATION, 2008, 85 (07) :923-927
[8]   Local extravascular pool of C3 is a determinant of postischemic acute renal failure [J].
Farrar, Conrad A. ;
Zhou, Wuding ;
Lin, Tao ;
Sacks, Steven H. .
FASEB JOURNAL, 2006, 20 (02) :217-226
[9]   CD46-induced human Treg enhance B-cell responses [J].
Fuchs, Anja ;
Atkinson, John P. ;
Fremeaux-Bacchi, Veronique ;
Kemper, Claudia .
EUROPEAN JOURNAL OF IMMUNOLOGY, 2009, 39 (11) :3097-3109
[10]   Human C3 deficiency associated with impairments in dendritic cell differentiation, memory B cells, and regulatory T cells [J].
Ghannam, Arije ;
Pernollet, Martine ;
Fauquert, Jean-Luc ;
Monnier, Nicole ;
Ponard, Denise ;
Villiers, Marie-Bernadette ;
Peguet-Navarro, Josette ;
Tridon, Arlette ;
Lunardi, Joel ;
Gerlier, Denis ;
Drouet, Christian .
JOURNAL OF IMMUNOLOGY, 2008, 181 (07) :5158-5166