Antibody-mediated organ-allograft rejection

被引:341
作者
Colvin, RB [1 ]
Smith, RN [1 ]
机构
[1] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Pathol, Cambridge, MA 02140 USA
关键词
D O I
10.1038/nri1702
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:807 / 817
页数:11
相关论文
共 124 条
  • [51] Interstitial rejection, vascular rejection, and diffuse thrombosis of renal allografts - Predisposing factors, histology, immunohistochemistry, and relation to outcome
    KooijmansCoutinho, MF
    Hermans, J
    Schrama, E
    Ringers, J
    Daha, MR
    Bruijn, JA
    vanderWoude, FJ
    [J]. TRANSPLANTATION, 1996, 61 (09) : 1338 - 1344
  • [52] Description of B lymphocytes and plasma cells, complement, and chemokines/receptors in acute liver allograft rejection
    Krukemeyer, MG
    Moeller, J
    Morawietz, L
    Rudolph, B
    Neumann, U
    Theruvath, T
    Neuhaus, P
    Krenn, V
    [J]. TRANSPLANTATION, 2004, 78 (01) : 65 - 70
  • [53] Endothelial cell chimerism after renal transplantation and vascular rejection
    Lagaaij, EL
    Cramer-Knijnenburg, GF
    van Kemenade, FJ
    van Es, LA
    Bruijn, JA
    van Krieken, JHJM
    [J]. LANCET, 2001, 357 (9249) : 33 - 37
  • [54] Impact of humoral alloreactivity early after transplantation on the long-term survival of renal allografts
    Lederer, SR
    Kluth-Pepper, B
    Schneeberger, H
    Albert, E
    Land, W
    Feucht, HE
    [J]. KIDNEY INTERNATIONAL, 2001, 59 (01) : 334 - 341
  • [55] All chronic rejection failures of kidney transplants were preceded by the development of HLA antibodies
    Lee, PC
    Terasaki, PI
    Takemoto, SK
    Lee, PH
    Hung, CJ
    Chen, YL
    Tsai, A
    Lei, HY
    [J]. TRANSPLANTATION, 2002, 74 (08) : 1192 - 1194
  • [56] Risk factors for capillary C4d deposition in kidney allografts:: Evaluation of a large study cohort
    Lorenz, M
    Regele, H
    Schillinger, M
    Exner, M
    Rasoul-Rockenschaub, S
    Wahrmann, M
    Kletzmayr, J
    Silberhumer, G
    Hörl, WH
    Böhmig, GA
    [J]. TRANSPLANTATION, 2004, 78 (03) : 447 - 452
  • [57] Monocytes and peritubular capillary C4d deposition in acute renal allograft rejection
    Magil, AB
    Tinckam, K
    [J]. KIDNEY INTERNATIONAL, 2003, 63 (05) : 1888 - 1893
  • [58] Use of C4d as a diagnostic adjunct in lung allograft biopsies
    Magro, CM
    Harman, AP
    Klinger, D
    Orosz, C
    Adams, P
    Waldman, J
    Knight, D
    Kelsey, M
    Ross, P
    [J]. AMERICAN JOURNAL OF TRANSPLANTATION, 2003, 3 (09) : 1143 - 1154
  • [59] MAINTENANCE OF SKIN XENOGRAFTS OF WIDELY DIVERGENT PHYLOGENETIC ORIGIN ON CONGENITALLY ATHYMIC (NUDE) MICE
    MANNING, DD
    REED, ND
    SHAFFER, CF
    [J]. JOURNAL OF EXPERIMENTAL MEDICINE, 1973, 138 (02) : 488 - 494
  • [60] Decay-accelerating factor induction on vascular endothelium by vascular endothelial growth factor (VEGF) is mediated via a VEGF receptor-2 (VEGF-R2)- and protein kinase C-α/ε (PKC α/ε)-dependent cytoprotective signaling pathway and is inhibited by cyclosporin A
    Mason, JC
    Steinberg, R
    Lidington, EA
    Kinderlerer, AR
    Ohba, M
    Haskard, DO
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (40) : 41611 - 41618