Abe A, Ishizu A, Fugo K, Ikeda H, Yoshiki T
Department of Pathology/Pathophysiology, Division of Pathophysiological Science, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Clin Exp Rheumatol. 2006 May-Jun;24(3):313-6.
Human T cell leukemia virus type I env-pX transgenic rats (env-pX rats) were used to investigate the pathogenesis of arthritis.
Phenotype of cells infiltrated into arthritic joints in env-pX rats was analyzed using flow cytometry and cell-transfer experiments were done using env-pX and wild-type WKAH rats.
The majority of T cells infiltrated into arthritic joints in env-pX rats exhibited a CD4 and activated phenotype. Transfer of these T cells into articular space in wild-type WKAH rats succeeded to induce arthritis similarly seen in env-pX rats. However, injection of the cells into sites other than joints did not induce inflammation. Transfer of in vitro-stimulated lymph node cells from disease-free env-pX rats into articular space did not induce arthritis in wild-type WKAH rats.
These findings suggest that articular tissues carrying the env-pX transgene are required for generation of arthritogenic T cells in env-pX rats. However, the constitutive antigens other than the transgene products are recognized as immunological targets by the arthritogenic T cells in the advanced arthritic joints. Molecules expressed specifically in articular tissues may be needed to maintain the inflammatory cell infiltration.
利用人I型T细胞白血病病毒env-pX转基因大鼠（env-pX大鼠）研究关节炎的发病机制。
采用流式细胞术分析env-pX大鼠关节炎关节中浸润细胞的表型，并使用env-pX大鼠和野生型WKAH大鼠进行细胞转移实验。
浸润到env-pX大鼠关节炎关节中的大多数T细胞表现出CD4和活化表型。将这些T细胞转移到野生型WKAH大鼠的关节腔中成功诱导出了与env-pX大鼠相似的关节炎。然而，将细胞注射到关节以外的部位并未诱发炎症。将来自无病env-pX大鼠的体外刺激的淋巴结细胞转移到野生型WKAH大鼠的关节腔中并未诱发关节炎。
这些发现表明，携带env-pX转基因的关节组织是env-pX大鼠中致关节炎T细胞产生所必需的。然而，除转基因产物外的组成性抗原在晚期关节炎关节中被致关节炎T细胞识别为免疫靶点。可能需要关节组织中特异性表达的分子来维持炎症细胞浸润。
