Role of anti-HLA antibodies in allograft rejection

  • Hong Bian
  • Paul E. Harris
  • Elaine F. Reed
Part of the Transplantation and Clinical Immunology book series (TRAC, volume 29)


It is well recognized that pre-existing antibodies to HLA antigens expressed by the allograft is detrimental to survival of kidney allografts and results in hyperacute and accelerated rejection [1]. Furthermore, it has been shown that heart and liver transplant recipients with pre-existing anti-donor HLA antibodies experience lower graft survival than patients without anti-donor anti-HLA antibodies [2, 3]. In hyperacute rejection, the injury occurs immediately, and the classical pathological features are infiltrating neutrophils, fibrinoid necrosis, and platelet thrombi. Fortunately, the occurrence of this type of rejection has been largely reduced by performing a pretransplant cross-match with the donor. The role of anti-HLA antibodies in chronic rejection is less well understood. Chronic rejection is the major limiting factor to long-term survival of organ allografts [4, 5, 6]. It is responsible for the loss of 50% of kidney allografts and 45% of cardiac allografts by 5 years after transplantation. The graft survival rates for other organ transplants generally show comparable results, with the exception of liver, which seems somewhat better tolerated. Chronic rejection, is defined as progressive functional deterioration of transplanted tissue occurring months or years after engraftment. The hallmark of chronic rejection is accelerated graft atherosclerosis which is characterized by diffuse, concentric, intimai occlusive lesions leading to gradual fibrosis of the transplanted organ [4, 5, 6].


Fibroblast Growth Factor Receptor Chronic Rejection Hyperacute Rejection Progressive Functional Deterioration Chronic Vascular Rejection 
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© Kluwer Academic Publishers 1997

Authors and Affiliations

  • Hong Bian
  • Paul E. Harris
  • Elaine F. Reed

There are no affiliations available

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