Zusammenfassung
Rejection involves cell- and antibody-mediated organ injury occurring as the result of recognition of an allograft as nonself. This process is categorized histologically and immunologically into three major types: hyperacute, acute and chronic. Hyperacute rejection is mediated by pre-existing antibodies to allogeneic antigens on the vascular endothelial cells within the donor organ. Donor recipient human leukocyte antigen (HLA) and ABO blood-group cross-matching are used to prevent hyperacute rejection [2]. Acute rejection is primarily a cell-mediated process that most commonly occurs from the first week to several years after transplantation. After heart transplantation [24], 61% of patients remain rejection free after the first posttransplantation month, 38% of patients are without rejection by 6 months, and 34% of patients are without rejection by 2 months. The hazard function for initial rejection peaks at approximately 1 month. Chronic rejection, or late graft failure, is an irreversible gradual deterioration of graft function that occurs in many allografts months to years after transplantation as the result of intimal thickening and fibrosis [2]. Cardiac allograft vasculopathy is angiographically evident in ≤45% of heart transplant recipients who survive ≥3 years [39]. This form of rejection involves a variety of immunesystem components: T cells, cytokines, macrophages, and adhesion molecules [3].
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Mueller, X.M. et al. (2002). lnterleukin-2 receptor antibodies for cardiac allograft. In: Rüter, F., von Scheidt, W., Buser, P., Zerkowski, HR. (eds) Thorakale Organtransplantation. Steinkopff, Heidelberg. https://doi.org/10.1007/978-3-642-57513-6_8
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DOI: https://doi.org/10.1007/978-3-642-57513-6_8
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