Gopal S, Narasimhan U, Day J D, Gao R, Kasper E K, Chen C L, Cina S, Robertson A L, Hruban R H
Department of Medicine, Stanford University Medical Center, California, USA.
Pathol Int. 1998 Mar;48(3):191-8. doi: 10.1111/j.1440-1827.1998.tb03892.x.
Quilty lesions, as first described by Billingham in 1981, or 'Quilty Effect' (QE) are distinct endomyocardial mononuclear cell infiltrates that have been observed in human heart transplant recipients, as well as in experimental models of heart transplantation. In the present investigations, the pattern and extent of apoptosis (programmed cell death) and myocyte necrosis, as well as specific lymphocyte subsets in Quilty lesions was assessed. Endomyocardial biopsies obtained from 13 patients at 10-3362 days post-transplant were examined. Apoptosis, as identified by DNA nick end-labeling, was found in myocytes at the periphery of Quilty lesions in 11 of 13 cases (85%), and 'early' stages of myocyte necrosis, as demonstrated by specific staining with alpha light chain myosin monoclonal antibodies (mAb), was observed at the same sites in 10 of 13 cases (77%) of both Quilty type A and type B lesions. Apoptosis was not identified in the lymphocyte infiltrates of any of the lesions examined. Lymphocyte subsets were characterized using mAb for T cell receptor (CD3), for helper/inducer T cells (CD4), for cytotoxic/suppressor T cells (CD8) and for mature B cells (CD20). Immunostaining revealed separate clusters of T lymphocytes with less prevalent B cells within the Quilty lesions. CD4+ cells were found in larger numbers than CD8+ cells in all cases. Non-B, non-T large lymphocytes were occasionally present. Except for the extent of the cellular infiltrate, no major cytochemical lymphocyte distribution differences were found between Quilty type A and B lesions. Myocyte apoptosis and early necrosis at the periphery of Quilty lesions suggest that early myocyte injury occurring in B lesions may represent initial or 'abortive stages' of cardiac allograft rejection. Why these lesions do not progress to overt rejection indeed warrant further detailed studies.
奎尔蒂病变（Quilty lesions），由比林厄姆（Billingham）于1981年首次描述，即“奎尔蒂效应”（QE），是在人类心脏移植受者以及心脏移植实验模型中观察到的明显的心内膜下单核细胞浸润。在本研究中，评估了奎尔蒂病变中细胞凋亡（程序性细胞死亡）和心肌细胞坏死的模式及程度，以及特定淋巴细胞亚群。对13例患者在移植后10至3362天获取的心内膜活检组织进行了检查。通过DNA缺口末端标记鉴定的细胞凋亡，在13例中的11例（85%）奎尔蒂病变周边的心肌细胞中被发现，并且通过α轻链肌球蛋白单克隆抗体（mAb）特异性染色显示的心肌细胞坏死“早期”阶段，在13例中的10例（77%）的奎尔蒂A型和B型病变的相同部位被观察到。在所检查的任何病变的淋巴细胞浸润中均未发现细胞凋亡。使用针对T细胞受体（CD3）、辅助/诱导性T细胞（CD4）、细胞毒性/抑制性T细胞（CD8）和成熟B细胞（CD20）的单克隆抗体对淋巴细胞亚群进行了表征。免疫染色显示奎尔蒂病变内有单独的T淋巴细胞簇，B细胞较少见。在所有病例中，发现CD4 +细胞的数量多于CD8 +细胞。偶尔会出现非B、非T大淋巴细胞。除了细胞浸润程度外，在奎尔蒂A型和B型病变之间未发现主要的细胞化学淋巴细胞分布差异。奎尔蒂病变周边的心肌细胞凋亡和早期坏死表明，B病变中发生的早期心肌细胞损伤可能代表心脏同种异体移植排斥反应的初始或“流产阶段”。这些病变为何未进展为明显的排斥反应确实值得进一步详细研究。
