Seko Y, Sato O, Takagi A, Tada Y, Matsuo H, Yagita H, Okumura K, Yazaki Y
Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
Circulation. 1996 May 15;93(10):1788-90. doi: 10.1161/01.cir.93.10.1788.
Infiltration by perforin-secreting killer lymphocytes, such as T cells and natural killer cells, has been shown to be involved in the pathogenesis of vascular cell damage in Takayasu's arteritis.
To investigate the immunological mechanisms involved, especially the nature of T-cell infiltration in Takayasu's arteritis as well as atherosclerosis, we analyzed the expression of T-cell receptor (TCR) Valpha and Vbeta genes in infiltrating cells in the aortic tissue of patients with Takayasu's arteritis and the atherosclerotic aortic aneurysm by polymerase chain reaction (PCR). We also analyzed the expression of cytokine genes by PCR. We found that the repertoires of TCR Valpha as well as Vbeta gene transcripts in Takayasu's arteritis were restricted. The infiltrating cells expressing Valpha2, Valpha16, Valpha17, Vbeta7, and Vbeta13.1 were found in 3 of 4 patients. In contrast, TCR Valpha-Vbeta repertoires in atherosclerotic aortic aneurysm were polyclonal. There was no significant difference in the pattern of cytokine gene expression between the two diseases.
The restricted usage of TCR Valpha as well as Vbeta genes by infiltrating T cells in Takayasu's arteritis may indicate that a specific antigen in the aortic tissue was targeted. Our findings provide the evidence that distinct immunological mechanisms are involved in the pathogenesis of Takayasu's arteritis and atherosclerotic aortic aneurysm.
分泌穿孔素的杀伤淋巴细胞（如T细胞和自然杀伤细胞）的浸润已被证明参与了大动脉炎血管细胞损伤的发病机制。
为了研究其中涉及的免疫机制，特别是大动脉炎以及动脉粥样硬化中T细胞浸润的性质，我们通过聚合酶链反应（PCR）分析了大动脉炎患者和动脉粥样硬化性主动脉瘤患者主动脉组织中浸润细胞的T细胞受体（TCR）Vα和Vβ基因的表达。我们还通过PCR分析了细胞因子基因的表达。我们发现，大动脉炎中TCR Vα以及Vβ基因转录本的库是受限的。在4例患者中的3例中发现了表达Vα2、Vα16、Vα17、Vβ7和Vβ13.1的浸润细胞。相比之下，动脉粥样硬化性主动脉瘤中的TCR Vα-Vβ库是多克隆的。两种疾病之间细胞因子基因表达模式没有显著差异。
大动脉炎中浸润的T细胞对TCR Vα以及Vβ基因的使用受限可能表明主动脉组织中的一种特定抗原是靶点。我们的发现提供了证据，表明不同的免疫机制参与了大动脉炎和动脉粥样硬化性主动脉瘤的发病机制。
