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首页> 外文期刊>Journal of the Neurological Sciences: Official Bulletin of the World Federation of Neurology >Flow cytometry evaluation of the T-cell receptor Vbeta repertoire among human T-cell lymphotropic virus type-1 (HTLV-1) infected individuals: effect of interferon alpha therapy in HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP).
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Flow cytometry evaluation of the T-cell receptor Vbeta repertoire among human T-cell lymphotropic virus type-1 (HTLV-1) infected individuals: effect of interferon alpha therapy in HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP).

机译:流式细胞术评估人类T细胞淋巴病毒1型(HTLV-1)感染的个体中T细胞受体Vbeta组成部分:干扰素α治疗在HTLV-1相关性脊髓病/热带痉挛性轻瘫(HAM / TSP)中的作用。

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Human T-cell lymphotropic virus type-1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is chronic inflammatory disease of the spinal cord characterized by perivascular lymphocytic cuffing and parenchymal lymphocytic infiltration. In this study using flow cytometry, we have investigated the T-cell receptor (TCR) Vbeta repertoire of peripheral blood T lymphocytes in 8 HAM/TSP patients, 10 HTLV-1 infected healthy carriers, and 11 uninfected healthy controls to determine if there is a biased usage of TCR Vbeta. We found that TCR Vbeta7.2 was under-utilized and Vbeta12 was over-utilized in CD4+ T cells of HTLV-1 infected individuals compared with healthy uninfected controls, whereas there were no such differences in CD8+ T cells. Comparison of Vbeta repertoire changes before and after interferon-alpha (IFN-alpha) treatment for HAM/TSP revealed that one out of five patients showed dramatic decrease of specific Vbeta in CD8+ T cells. Our results suggest that dominant Vbeta subpopulationsin CD4+ T cells evolved associated with chronic HTLV-1 infection, and IFN-alpha treatment for HAM/TSP does not induce a specific pattern of TCR Vbeta changes.
机译:与人类T细胞1型淋巴细胞性病毒(HTLV-1)相关的脊髓病/热带痉挛性轻瘫(HAM / TSP)是脊髓的慢性炎症性疾病,其特征在于血管周淋巴细胞套扎和实质性淋巴细胞浸润。在这项使用流式细胞仪的研究中,我们调查了8例HAM / TSP患者,10例HTLV-1感染的健康携带者和11例未感染的健康对照者的外周血T淋巴细胞的T细胞受体(TCR)Vbeta组成,以确定是否存在TCR Vbeta的用法有偏见。我们发现与健康的未感染对照相比,HTLV-1感染者的CD4 + T细胞中TCR Vbeta7.2的利用不足,而Vbeta12被过度利用,而CD8 + T细胞中则没有这种差异。比较HAM / TSP干扰素-α(IFN-α)治疗前后的Vbeta库变化,发现五分之一的患者CD8 + T细胞中特异性Vbeta明显降低。我们的结果表明,与慢性HTLV-1感染相关的CD4 + T细胞中主要的Vbeta亚群进化而来,而HAM / TSP的IFN-α治疗则不会诱导TCR Vbeta改变的特定模式。

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