Boldt-Houle D M, Rinaldo C R, Ehrlich G D
Department of Pathology, University of Pittsburgh School of Medicine, Pennsylvania 15261.
J Leukoc Biol. 1993 Nov;54(5):486-91. doi: 10.1002/jlb.54.5.486.
A cross-sectional PCR analysis of the TCR V beta repertoires in HIV-1 seronegative controls and HIV-1 infected individuals with either clinically or immunologically defined AIDS [1] was performed to examine the proposed superantigen model for HIV-1 pathogenesis. In contrast to previous reports, we find neither uniform specific losses nor uniform clonal expansions of particular TCR V beta gene families in subjects with AIDS. Instead our study, which was designed specifically to qualitatively determine the presence or absence of TCR V beta families in both subject populations, indicates an overall diminution in the expression of TCR V beta gene families in HIV-1 infected individuals with AIDS compared with controls. This is commensurate with the decrease in CD4 T cells in the AIDS population. Our data are therefore not directly suggestive of a common superantigen model of HIV-1 induced T cell clonal depletion or anergy, but instead emphasize a broad decrease in signals throughout the TCR V beta repertoire in AIDS versus control groups. This random depletion in the TCR V beta repertoire is most likely caused by aspects of HIV-1 pathogenesis other than virus-encoded superantigens.
对人类免疫缺陷病毒1型（HIV-1）血清学阴性对照者以及临床或免疫学确诊为艾滋病的HIV-1感染者的T细胞受体Vβ库进行了横断面聚合酶链反应（PCR）分析，以检验所提出的HIV-1发病机制的超抗原模型。与之前的报道不同，我们发现艾滋病患者中特定的TCR Vβ基因家族既没有一致的特异性缺失，也没有一致的克隆性扩增。相反，我们的研究专门设计用于定性确定这两类人群中TCR Vβ家族的存在与否，结果表明，与对照组相比，患有艾滋病的HIV-1感染者中TCR Vβ基因家族的表达总体减少。这与艾滋病患者群体中CD4 T细胞的减少是一致的。因此，我们的数据并不直接支持HIV-1诱导T细胞克隆耗竭或无反应性的常见超抗原模型，而是强调与对照组相比，艾滋病组整个TCR Vβ库中的信号普遍减少。TCR Vβ库中的这种随机耗竭很可能是由HIV-1发病机制中除病毒编码超抗原之外的其他因素引起的。
