Nádasdy T, Kemény E, Krenács T, Csajbók E, Szenohradszky P, Stiller D, Ormos J
Department of Pathology, Szent-Györgyi Albert Medical University, Szeged, Hungary.
Acta Morphol Hung. 1991;39(3):187-99.
Arteries were investigated ultrastructurally in material from 40 needle and wedge biopsies of renal allografts, and immunohistochemically in another 10 cases with signs of chronic obliterative transplantation arteriopathy. In the early biopsies, but even in the control kidneys, thin extensions of the smooth muscle cells of the media were observed, which were in direct contact with the endothelial cells through the lamina elastica interna. These extensions may contain receptors mediating endothelial noxae to the smooth muscle cells thus initiating their proliferation, migration to the intima presumably begins in the early post-transplant period and continues until the lumen is occluded. Concomitantly, inflammatory cells (mainly macrophages, with a smaller number of CD4 and CD8-positive T lymphocytes) invade the intima. The proliferating myointimal cells, possibly having become HLA-DR-positive, may behave as antigen-presenting cells, enhancing the anti-graft immune response further, and aggravating the arterial injury.
对40例同种异体肾移植针吸活检和楔形活检材料的动脉进行了超微结构研究，并对另外10例有慢性闭塞性移植性动脉病迹象的病例进行了免疫组织化学研究。在早期活检中，甚至在对照肾中，都观察到中膜平滑肌细胞的细延伸部分，它们通过内弹性膜与内皮细胞直接接触。这些延伸部分可能含有介导内皮损伤信号传递给平滑肌细胞的受体，从而启动其增殖，内膜迁移大概在移植后早期开始并持续到管腔闭塞。同时，炎症细胞（主要是巨噬细胞，少量CD4和CD8阳性T淋巴细胞）侵入内膜。增殖的肌内膜细胞可能已成为HLA-DR阳性，可能表现为抗原呈递细胞，进一步增强抗移植免疫反应，并加重动脉损伤。
