SEQUENTIAL IMMUNOLOGICAL TARGETING OF CHRONIC EXPERIMENTAL ARTERIAL ALLOGRAFT
SEQUENTIAL IMMUNOLOGICAL TARGETING OF CHRONIC EXPERIMENTAL ARTERIAL ALLOGRAFT
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DOI：
10.1097/00007890-199509000-00003
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发表时间：
1995-09-15
期刊：
影响因子：
6.2
通讯作者：
MICHEL, JB
中科院分区：
文献类型：
--
作者：
PLISSONNIER, D;NOCHY, D;MICHEL, JB
动脉壁是慢性排斥反应的主要部位。本研究采用大鼠腹主动脉同种异体移植模型，描述了动脉移植排斥反应中动脉壁免疫损伤和反应的不同靶点和效应物的顺序演变。内皮和平滑肌细胞损伤和体液和细胞免疫效应的特点是从0至60天后移植使用电池的特异性抗体。内膜增殖反应也在这段时间内进行了表征。同种移植的Brown-Norway主动脉外膜的细胞成分非常少，这表明供体外膜在同种异体移植物中的抗原性较差。相比之下，同种异体移植物外膜是一个主要的炎症细胞入侵的网站，其中的粘附分子的表达，通过殖民毛细血管内皮细胞可以发挥主要作用。只要中膜平滑肌持续存在，这种外膜浸润就会持续。腔内皮细胞早期消失，可能与巨噬细胞边缘化有关。相反，中膜平滑肌细胞消失发生较晚，并被免疫球蛋白特异性靶向。内膜增殖是最迟的现象，包括早期的炎性细胞浸润和后期的肌纤维母细胞增殖，并且可能与该层中生长因子的特异性表达有关。大鼠主动脉同种异体移植物模型对于表征慢性动脉移植物排斥的特异性靶点和效应物是有用的，表明内皮损伤的早期阶段和涉及慢性中膜平滑肌细胞损伤的免疫球蛋白的存在。
Arterial wall is the main site involved in the chronic rejection process. The rat aortic allograft model was used here to characterize and describe the sequential evolution of the different targets and effecters of arterial wall immunological injury and response during arterial allograft rejection.Rat abdominal aortae were isografted or allografted from Brown-Norway to Lewis rats. Endothelial and smooth muscle cell injury and humoral and cellular immunological effecters were characterized from 0 to 60 days after transplantation using a battery of specific antibodies. The intimal proliferative response was also characterized over this time.Isografted Brown-Norway aorta adventitia had very few cellular components, which suggests that donor adventitia would be poorly antigenic in allografts. In contrast, allograft adventitia was the site of a major inflammatory cell invasion in which the expression of an adhesion molecule by colonizing capillary endothelial cells could play a main role. This adventitial infiltration continued as long as medial smooth muscle persisted. The luminal endothelial cells disappeared early, probably associated with macrophage margination. In contrast, medial smooth muscle cell disappearance occurred later and was specifically targeted by immunoglobulins. Intimal proliferation was the most delayed phenomenon, involving both inflammatory cell infiltration at an early stage and later myofibroblastic proliferation, and could be related to the specific expression of growth factors in this layer.The rat aortic allograft model appeared useful for characterizing specific targets and effecters of chronic arterial graft rejection, demonstrating an early stage of endothelial injury and the presence of immunoglobulins involved in chronic medial smooth muscle cell injury.