Studies on Immunobiological Mechanisms in Atherogenesis

（1）为了利用T细胞-宏观效应在生育中的作用，我们研究了T细胞-分化的运动同源性（rnu/rnu）大鼠诱导胆固醇-富集的饮食中T细胞和宏观效应的分布模式。在与运行/...老鼠的比较中，狮子座的发展是有限的。在微观宏观上的泡沫细胞转变在rnu/rnu老鼠中表现得更好。（2）我们从抗原家族中发现了一个细胞，该细胞展示了大动脉内的牙科细胞。这些血管牙科细胞（VDC）常见于运动clerotic lesions，以及快速CDla和S-100。目前在VDC Birbeck颗粒状结构的细胞系中被披露，该结构独特地出现在Langerhans细胞中。使用Lag antibody的进一步研究。在Langerhans细胞中，特别地发现了生物桶颗粒和生物桶颗粒相关的结构，其中较低的阳性细胞在aortic wall中被发现。The Findings Watained Mayimply，即antigen presentaion migh的机制与那些在atherosclerosis中的参与相似。（3）我们证明ICAM-1表达是在饮食诱导的高胆固醇大鼠中对胆固醇区域进行了调整的。[CAM-1与增强型宏观微观重构有关的增加表达式。反ICAM-1/LFA-1 mab减少了巨噬生长及其迁移到其内部。这些结果建议，ICAM-1/LFA-1路径在胆固醇诱导性凋亡早期阶段中发生了宏观-内细胞相互作用。（4）使用三个维度培养模型模拟体内植物。我们提供了证据，即nLDLs和氧化LDLs可以作为ET-1在高脂血症和动脉粥样硬化中增加释放的潜在中介。

(1) To elucidate the role of T cell-macrophage interactions in atherogeness we studied the distribution pattern of T cells and macrophages in T cell-depleted athymic homozygous (rnu/rnu) rats fed a cholesterol-enriched diet. In comparison with run/・・・rats, the lesion development was limited in size. whereas foam cell transformation of intimal macrophages was more prominent in rnu/rnu rats. (2) We found that cells from the family of antigen presenting dendritic cells reside in the intima of large arteries. These vascular dendritic cells (VDC) are common in atherosclerotic lesions, and express CDla and S-100. Present ultrastructural examination disclosed in the cytoplasm of VDC Birbeck granule-like structures that are uniquely present in Langerhans cells. Further studies using Lag antibody. which specifically stains Bioreck granules and Biobeck granule-associated structures in Langerhans cells demonstrated that Lag-positive cells were found in the aortic wall. The findings obtained mayimply that mechanisms of antigen presentaion migh be similar to those involved in atherosclerosis. (3) We demonstrated that ICAM-1 expression is up-regulated in the lesionprone areas of aorta in diet-induced hypercholesterolemic rats. Increased expression of [CAM-1 was associated with enhanced macrophage intimal recruitment. Injection of anti-ICAM-1/LFA-1 mab reduced macrophage adherence and their migration into the intima. These results suggest that the ICAM-1/LFA-1 pathway is involved in macrophage-endothelial cell interactions during the early stage of cholesterol-induced atherogenesis. (4) Using a three dimensional culture model simulating in vivo arterial intima. we provided evidence that nLDLs and oxidized LDLs may act as a potential mediator for the increased release of ET-1 in hyperlipidemia and atherosclerosis.