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The alloimmune response of the recipient against the transplanted heart can injure the constituent cells of the graft, impairing their function[1]. The potential target cells for injury include not only the myocytes, whose destruction forms the basis for rejection surveillance and treatment, but also the cells of the vasculature, which provide the interface between donor and recipient. The alloimmune response involves the presentation of donor antigen, by vascular endothelial cells and/or by passenger leukocytes, leading to the activation and clonal proliferation of T cells that specifically recognize alloantigens[1] (Chapter 7). These events, as well as recruitment of macrophages and the up-regulation of cell surface antigens for adhesion of inflammatory cells, lead to the release of cytokines and the up-regulation of their receptors. The consequence of these events is the release of powerful biologic effectors of cell injury[1]. Myocyte injury and necrosis occurring during this process are readily recognized by histologic examination, and form the cornerstone of rejection surveillance in heart transplant (HTx) recipients. |
