Increased activated human T cell lymphotropic virus type I (HTLV-I) tax11-19-specific memory and effector CD8+ cells in patients with HTLV-I-associated myelopathy/tropical spastic paraparesis:: Correlation with HTLV-I provirus load
Increased activated human T cell lymphotropic virus type I (HTLV-I) tax11-19-specific memory and effector CD8+ cells in patients with HTLV-I-associated myelopathy/tropical spastic paraparesis:: Correlation with HTLV-I provirus load
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DOI：
10.1086/317932
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发表时间：
2001-01-15
影响因子：
6.4
通讯作者：
Jacobson, S
中科院分区：
文献类型：
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作者：
Nagai, M;Kubota, R;Jacobson, S
为了辨别与T细胞分化相关的T细胞亚型，从HTLV-I相关性脊髓病/热带痉挛性轻瘫（HAM/TSP）患者外周血淋巴细胞中的总CD 8（高）细胞和人T细胞嗜淋巴病毒I型（HTLV-I）Tax 11 -19肽特异性CD 8（+）细胞中测量CD 45 RA和CD 27的表达。与HTLV-I血清阴性健康对照受试者相比，HAM/TSP CD 8（+）细胞中表型定义的记忆和/或效应细胞（CD 45 RA（-）CD 27（+）、CD 45 RA（+）CD 27（-）和CD 45 RA（-）CD 272（-））增加。HAM/TSP组CD 8（+）细胞中HLA DR阳性细胞百分率也高于健康对照组CD 8（+）细胞中HLA DR阳性细胞百分率。HTLV-I前病毒载量与Tax 11 -19特异性CD 8（+）细胞的频率相关。高频率的记忆和/或效应型HTLV-I Tax 11 -19特异性CD 8（+）细胞表明，体内由HTLV-I抗原驱动的持续再刺激可能与HAM/TSP的发病机制相关。
To discern the T cell subtype associated with T cell differentiation, the expression of CD45RA and CD27 was measured from total CD8(high) cells and from human T cell lymphotropic virus type I (HTLV-I) Tax11-19 peptide-specific CD8(+) cells in peripheral blood lymphocytes of patients with HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Phenotypically defined memory and/or effector cells (CD45RA(-)CD27(+), CD45RA(+)CD27(-), and CD45RA(-)CD272(-)) were increased in HAM/TSP CD8(+) cells, compared with those of HTLV-I-seronegative healthy control subjects. The percentage of human leukocyte antigen (HLA)-DR-positive cells was also increased in CD8(+) cells of HAM/TSP, compared with those in HLA-DR(+)CD8(+) cells of healthy control subjects. HTLV-I provirus load correlated with the frequency of Tax11-19-specific CD8(+) cells. The high frequency of memory and/or effector type HTLV-I Tax11-19-specific CD8(+) cells suggests that continuous restimulation driven by HTLV-I antigens in vivo may be associated with the pathogenesis of HAM/TSP.