移植肾动脉病变的免疫金电镜观察

Investigation of arteriopathy of renal allograft by immuno-gold electron microscope

  • 摘要: 目的:观察移植肾动脉病的超微结构形态,探讨移植肾动脉病的发生机制。方法:应用Lowicryl K4M(K4M)低温包埋、免疫金标记的透射电镜技术观察了5例发生移植肾动脉病的肾动脉内膜形态改变,5例正常供肾肾动脉作为对照。结果:①内膜内皮细胞和平滑肌细胞异常表达Ⅱ类主要组织相容性抗原(HLA-D)。5例正常供肾肾动脉内膜内皮细胞和平滑肌细胞则呈阴性。②病变内膜中的主要成分为“合成型”平滑肌细胞及其细胞外基质。平滑肌细胞胞浆中除含有密斑、密体样结构外,还可见到丰富的粗面内质网,并表达核增殖基因c-myc蛋白。③内膜病变中T淋巴细胞与单核吞噬细胞各占65%与35%。④CD4阳性T与CD8阳性T淋巴细胞的数量基本相等,它们的超微结构形态十分相似,难以区分。⑤病变中未能发现CD20阳性的B淋巴细胞。结论:移植肾动脉病是内皮损伤后单核吞噬细胞、T淋巴细胞、平滑肌细胞之间通过HLA-D相互作用,从而形成了一种以平滑肌细胞增殖为主的动脉内膜炎

     

    Abstract: Objective: To study the ultrastructural features and HLA-D antigen expression in the pathogenesis of arteriopathy of renal allograft.Methods: Intimal lesions in renal arteries from 5 allografts were embedded with K4M and investigated by immuno gold electron microscope. The specimens of five normal donor renal artery served as control. Results: (1)There was aberrant expression of HLA-D antigen by both endothelial and smooth muscle cells of arteriopathy. (2)The main components of intimal lesion were the synthesized type smooth muscle cells, which characterized by abundant intracytoplasmic rough endoplasmic reticulum and c-myc gene protein expression, and their extracellular matrix. (3)About 65% of intimal inflammatory infiltrates were T lymphocytes and the other 35% were of macrophages. (4)The number of CD4 lymphocytes were equal to that of CD8 cells. The two subtypes of T lymphocyte shared similar morphologic features. (5)There was no CD20 positive B lymphocyte in the intimal lesions.Conclusions:The arteriopathy of renal allograft is a T-lymphocyte-mediated endotheliolitis triggered by intimal endothelial injury. The cellular interactions through HLA-D antigen among T lymphocytes, macrophages, and smooth muscle cells may result in intimal proliferation and arterial stenosis.

     

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