Hodara V L, Jeddi-Tehrani M, Grunewald J, Andersson R, Scarlatti G, Esin S, Holmberg V, Libonatti O, Wigzell H
Department of Immunology, Karolinska Institute, Stockholm, Sweden.
AIDS. 1993 May;7(5):633-8. doi: 10.1097/00002030-199305000-00004.
To analyse variation in T-cell receptor (TCR) V beta gene expression in T cells in HIV-infected individuals.
Because there are very few monoclonal antibodies available for studying TCR V beta gene expression, we used polymerase chain reaction (PCR) to analyse the TCR V beta repertoire in HIV-infected individuals using specific primers for 20 distinct families of TCR V beta.
Evaluation of TCR V beta gene expression in peripheral blood from HIV-1-infected individuals [two in Centers for Disease Control (CDC) stage II, five in CDC stage III and four in CDC stage IV]. Complementary DNA was produced from CD4+ and CD8+ T cells, amplified by PCR and analysed after Southern blotting and hybridization with a C beta-specific oligonucleotide probe.
V beta gene expression was dramatically modified, especially in AIDS patients. The CD4+ T-cell subset showed both overexpression (V beta 2) and deletions or underexpression (V beta 9-V beta 20), whereas these gene segments were expressed normally in the CD8+ subset. Only V beta 3 was deleted or underexpression in both CD4+ and CD8+ populations in AIDS patients.
HIV-1 infection induces CD4+ T-cell deficiency, both in total numbers and by causing a paucity of select V beta gene expression in this subset. In addition, the V beta 3 gene family was deleted or underexpressed was observed in both CD4+ and CD8+ T-cell subsets from patients in CDC stage IV. These results are compatible with changes in V beta gene expression known to occur under the action of endogenous or exogenous superantigens.
分析HIV感染个体T细胞中T细胞受体(TCR)Vβ基因表达的变化。
由于可用于研究TCR Vβ基因表达的单克隆抗体非常少,我们使用聚合酶链反应(PCR),用针对20个不同TCR Vβ家族的特异性引物分析HIV感染个体的TCR Vβ库。
评估HIV-1感染个体外周血中的TCR Vβ基因表达[疾病控制中心(CDC)II期2例,CDC III期5例,CDC IV期4例]。从CD4+和CD8+ T细胞产生互补DNA,通过PCR扩增,并在Southern印迹后用Cβ特异性寡核苷酸探针杂交进行分析。
Vβ基因表达发生了显著改变,尤其是在艾滋病患者中。CD4+ T细胞亚群既表现出过表达(Vβ2),又有缺失或低表达(Vβ9-Vβ20),而这些基因片段在CD8+亚群中正常表达。在艾滋病患者的CD4+和CD8+群体中,只有Vβ3缺失或低表达。
HIV-1感染导致CD4+ T细胞数量减少,并导致该亚群中特定Vβ基因表达缺乏。此外,在CDC IV期患者的CD4+和CD8+ T细胞亚群中均观察到Vβ3基因家族缺失或低表达。这些结果与已知在内源性或外源性超抗原作用下发生的Vβ基因表达变化相符。