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首页> 外文期刊>Journal of Translational Medicine >CD8 apoptosis may be a predictor of T cell number normalization after immune reconstitution in HIV
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CD8 apoptosis may be a predictor of T cell number normalization after immune reconstitution in HIV

机译：CD8凋亡可能是HIV免疫重建后T细胞数量正常化的预测指标

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Background As part of the Houston Vanguard study, a subset of 10 patients randomized to receive IL-2 therapy were compared to 4 patients randomized to not receive IL-2, for markers of T cell activation and death during the first three cycles of IL-2. All patients were treated with combination antiretroviral therapy (ART) and were virally suppressed. The purpose of the study was to examine the role of CD8+ T cell death in responses to ART and IL-2 therapy. Methods Lymphocytes were examined at Day 0, 5 and 30 days during three cycles of IL-2 therapy. CD25, CD38, HLA-DR expression and annexin (cell death) were examined on CD4 and CD8 subpopulations. Follow up studies examined CD4 levels and CD4:CD8 reconstitution after 6 years using both univariant and multivariate analyses. Results Human lymphocytes responded to IL-2 therapy by upregulation of CD25 on CD4+ T cells, leading to an increase in CD4 cell counts. CD8+ T cells did not increase CD25 expression, but upregulated activation antigens (CD38 and DR) and had increased death. At baseline, 7 of the 14 patients had high CD8+ T cell apoptosis (mean 17.0% ± 6.0). We did an exploratory analysis of immune status after six years, and found that baseline CD8+ T cell apoptosis was correlated with CD4 cell count gain beginning two years post enrollment. Patients with low levels of CD8+ T cell apoptosis at baseline (mean 2.2% ± 2.1) had significantly higher CD4 cell counts and more normalized CD4:CD8 ratios than patients with high CD8+ T cell apoptosis (mean CD4 cell counts 1,209 ± 164 vs 754 ± 320 cells/mm3; CD4:CD8 ratios 1.55 vs. 0.70, respectively). Conclusion We postulate that CD8+ T cell apoptosis may reflect inherent activation status, which continues in some patients even though viral replication is suppressed which influences the ability of CD4+ T cells to rebound. Levels of CD8+ T cell apoptosis may therefore be an independent predictor of immune status, which should be shown in a prospective study.
机译：背景作为休斯顿先锋研究的一部分，将10例随机接受IL-2治疗的患者与4例随机不接受IL-2的患者进行了比较，以了解IL-前三个周期中T细胞活化和死亡的标志物。 2。所有患者均接受抗逆转录病毒疗法（ART）联合治疗并被病毒抑制。该研究的目的是检验CD8 + T细胞死亡在ART和IL-2治疗反应中的作用。方法在IL-2治疗的三个周期中的第0、5和30天检查淋巴细胞。在CD4和CD8亚群上检查了CD25，CD38，HLA-DR表达和膜联蛋白（细胞死亡）。随访研究使用单变量和多变量分析对6年后的CD4水平和CD4：CD8重构进行了检查。结果人淋巴细胞通过上调CD4 + T细胞上CD25的表达而对IL-2治疗产生反应，导致CD4细胞计数增加。 CD8 + T细胞不增加CD25表达，但上调激活抗原（CD38和DR）并增加死亡。在基线时，这14例患者中有7例具有高CD8 + T细胞凋亡（平均17.0％±6.0）。我们对六年后的免疫状况进行了探索性分析，发现基线CD8 + T细胞凋亡与入选后两年开始的CD4细胞计数增加相关。基线时CD8 + T细胞凋亡水平低的患者（平均2.2％±2.1）比CD8 + + T细胞凋亡（平均CD4细胞计数为1,209±164比754±320细胞/ mm 3 ; CD4：CD8比分别为1.55和0.70）。结论我们推测CD8 + T细胞的凋亡可能反映了内在的激活状态，即使病毒复制受到抑制，影响CD4 + T细胞的能力，这种状态仍会持续。反弹。因此，CD8 + T细胞凋亡的水平可能是免疫状态的独立预测因子，应在前瞻性研究中证明。

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