Seko Y, Takahashi N, Tada Y, Yagita H, Okumura K, Nagai R
Department of Cardiovascular Medicine, Graduate School of Medicine, University of Tokyo, 113-8655, Tokyo, Japan.
Int J Cardiol. 2000 Aug 31;75 Suppl 1:S77-83; discussion S85-7. doi: 10.1016/s0167-5273(00)00194-7.
To further investigate the immunological mechanisms involved in Takayasu's arteritis, we analyzed the T-cell receptor (TCR) Vgamma and Vdelta gene usage by infiltrating gammadelta T-cells and the expression of costimulatory molecules B7-1, B7-2, CD40, CD27 ligand (CD27L), CD30L, OX40L in the arterial tissue of a patient with Takayasu's arteritis. We found that the repertoires of TCR Vgamma as well as Vdelta gene transcripts of the infiltrating cells were restricted as compared with those of peripheral blood lymphocytes from a patient with Takayasu's arteritis. This strongly suggests that gammadelta T-cells as well as alphabeta T-cells, as we previously reported, were specifically involved in the pathogenesis of Takayasu's arteritis. We also found that B7-1, B7-2, CD40, CD27L, CD30L, and OX40L were expressed in the arterial tissue, suggesting the roles for these costimulatory molecules in T-cell-mediated vascular injury in Takayasu's arteritis. Our findings strongly support the involvement of T-cell-mediated immunological mechanisms in the pathogenesis of Takayasu's arteritis.
为进一步研究大动脉炎所涉及的免疫机制，我们分析了1例大动脉炎患者动脉组织中浸润的γδ T细胞的T细胞受体（TCR）Vγ和Vδ基因使用情况以及共刺激分子B7-1、B7-2、CD40、CD27配体（CD27L）、CD30L、OX40L的表达。我们发现，与大动脉炎患者外周血淋巴细胞相比，浸润细胞的TCR Vγ以及Vδ基因转录谱受到限制。这有力地表明，正如我们之前报道的，γδ T细胞以及αβ T细胞均特异性参与了大动脉炎的发病机制。我们还发现B7-1、B7-2、CD40、CD27L、CD30L和OX40L在动脉组织中表达，提示这些共刺激分子在大动脉炎中T细胞介导的血管损伤中发挥作用。我们的研究结果有力地支持了T细胞介导的免疫机制参与大动脉炎发病过程。
