Mapping of vascular dendritic cells in atherosclerotic arteries suggests their involvement in local immune-inflammatory reactions
Mapping of vascular dendritic cells in atherosclerotic arteries suggests their involvement in local immune-inflammatory reactions
复制标题
DOI：
10.1016/s0008-6363(97)00229-0
复制
发表时间：
1998-03-01
影响因子：
10.8
通讯作者：
Lord, RSA
中科院分区：
文献类型：
--
作者：
Bobryshev, YV;Lord, RSA
目的：我们以前证明，血管树突状细胞（VDCs）存在于大动脉的内膜中，并且它们的数量在动脉粥样硬化病变中增加。本研究旨在确定VDC是否参与动脉粥样硬化形成中的免疫介导反应。方法：术中取颈动脉和主动脉标本。用抗CD 1a或S-100鉴定VDC。使用双重免疫染色程序研究了VDC与不同内膜细胞（包括T细胞和巨噬细胞）的共定位。在检测到共定位细胞的区域，检测HLA-DR、ICAM-1、VCAM-1表达的特异性。结果如下：在所有动脉粥样硬化斑块中，均观察到VDC与T细胞接触，但这些共定位细胞分布不规则，主要见于含有炎性浸润的新生血管形成区。在其他区域，很少检测到T细胞/VDC共定位，但经常发现VDC与巨噬细胞接触。在动脉粥样硬化病变下方的中膜和外膜中也检测到VDC，它们主要位于血管周围，特别是在表现出急性炎症体征的区域。在这些区域，VDC表达ICAM-1、VCAM-1，并与T细胞接触。在斑块和外膜中，具有共定位的VDC和T细胞的区域对应于具有HLA-DR表达的区域。结论：血管内皮细胞参与了动脉粥样硬化形成过程中T细胞的活化。VDC/T细胞共定位主要发生在动脉壁内的两个区域，即动脉粥样硬化病变内含有炎性浸润的新血管形成区域和外膜中血管周围的炎性浸润区域。可能的是，一些内膜VDC通过中膜和外膜迁移到邻近的淋巴结，在那里它们呈递动脉粥样硬化相关抗原。我们还推测VDC/巨噬细胞接触在动脉粥样硬化形成中处理免疫信息是必不可少的。(C)1998年Elsevier Science B.V.
Objective: We previously demonstrated that vascular dendritic cells (VDCs) are present in the intima of large arteries and that their numbers are increased in atherosclerotic lesions. This study was undertaken to determine whether VDC are involved in immune-mediated reactions in atherogenesis. Methods: Specimens of carotid artery and aorta were obtained at operation. VDCs were identified with anti-CD1a or with S-100. Co-localisation of VDCs with different intimal cells, including T-cells and macrophages, was studied using a double immunostaining procedure. In areas where the co-localising cells were detected, the peculiarities of expression of HLA-DR, ICAM-1, VCAM-1 were examined. Results: In all the atherosclerotic plaques, VDCs were seen in contact with T-cells, but these co-localising cells were irregularly distributed and were mainly found in zones of neovascularisation containing inflammatory infiltrates. In other areas, T-cell/VDC co-localisation was rarely detected but VDCs were often found in contact with macrophages. VDCs were detected also in the media beneath atherosclerotic lesions and in the adventitia, where they were mostly around vasa vasorum, especially in areas exhibiting signs of acute inflammation. In these areas VDCs expressed ICAM-1, VCAM-1 and were in contact with T-cells. In both plaques and in the adventitia, the areas with co-localising VDCs and T-cells corresponded to the areas with HLA-DR expression. Conclusions: The results suggest that VDCs are involved in T-cell activation in atherogenesis. There are two regions within the arterial wall where VDC/T-cell co-localisation mostly occurs, namely, in zones of neovascularisation containing inflammatory infiltrates located within atherosclerotic lesions, and in areas with inflammatory infiltrates around vasa vasorum in the adventitia. Possibly, some intimal VDCs migrate through the media and adventitia to adjacent lymph nodes where they present atherosclerosis associated antigens. We also speculate that VDC/macrophage contacts are essential in processing immune information in atherogenesis. (C) 1998 Elsevier Science B.V.