T cell surface antigen expression on lymphocytes of patients with AIDS during in vitro mitogen stimulation.

T cell surface antigen expression on lymphocytes of patients with AIDS during in vitro mitogen stimulation.
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体外有丝分裂原刺激期间艾滋病患者淋巴细胞上 T 细胞表面抗原的表达。

DOI:
10.1007/bf00205502
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发表时间:
1984
期刊:
Cancer immunology, immunotherapy : CII
影响因子:
--
通讯作者:
Newell,GR
Newell,GR
中科院分区:
--
文献类型:
--
作者:
Munn,CG;Reuben,JM;Hersh,EM;Mansell,PW;Newell,GR

文献摘要

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在8名艾滋病患者和8名正常人的PHA和pwm刺激培养中,每天检测外周血单核细胞(PBMC)表面标志物的表达。培养前,患者细胞表现出OKT 4+细胞减少(正常40.4%,患者22.3%,P<0.001)、OKT 8+细胞增加(正常27.6%,艾滋病38.4%,P=0.002)、OKT 10+细胞增加(正常15.5%,艾滋病42.8%,P=0.002)、HLA-DR+细胞增加(正常11.4%,艾滋病28.7%,P=0.01)的特点。两组的OKT 11+细胞比例在前2天内保持不变,而OKT 3+细胞比例在PHA中下降,而在PWM中没有下降(PHA:正常69.8%至35.1%;P=0.001,艾滋病56.5至38.5%;P=0.001, PWM:正常62.8%至65.9%,艾滋病66.8%至63.9%),两组在第5天恢复。在PWM培养中,okt3 +细胞在正常人中显著增加,而在艾滋病中没有增加(正常人62.6%-77.7%;P=0.04,艾滋病61.8 - 48.7%)。正常PHA培养1天后,okt4表达下降(38.9% ~ 29.6%;P=0.05),第5天恢复。在艾滋病PHA培养第5天,其表达增加(18.0% ~ 41.1%,P<0.001)。艾滋病培养中okt4 +细胞的最终百分比在正常范围内(35.0%-49.0%)。两组患者经PHA刺激后okt8表达均升高(正常组29.5% ~ 50.4%,P=0.002,艾滋病组37.4% ~ 50.7%,P=0.02),经PWM刺激后正常组okt8表达升高(正常组28.9% ~ 35.5%,P=0.004,艾滋病组38.5% ~ 35.6%)。由于okt4和okt8表达的相对变化,正常PHA培养的4/8比值下降(1.89 ~ 1.03,P=0.1),艾滋病培养的4/8比值上升(0.68 ~ 1.18,P=0.09)。此外,在PHA培养中,okt4 +和okt8 +细胞的总数从68%增加到94%,而okt11的表达保持不变,表明这些抗原在单个细胞上共表达。PHA和PWM刺激的正常细胞okt10 (PHA 16.0% ~ 53.4%, P=0.01, PWM 16.1% ~ 33.9%, P=0.03)和HLA-DR (PHA 8.6% ~ 27.3%, P=0.03, PWM 12.5% ~ 26.6%, P=0.07)均升高。在艾滋病PHA培养中,这种情况没有改变,而在PWM培养中,okt10的表达下降(44.8%至23.0%;P=0.05)。PHA和PWM刺激的艾滋病患者培养结果显示,Tac的生成明显减少(正常人PHA从5.4%增加到77.1%,艾滋病从3.2%增加到48.0%,P=0.001;正常人PWM从6.1%增加到35.3%,艾滋病从5.0%增加到15.5%,P=0.04)。分析表明,这种缺陷仅限于小淋巴细胞的表达减少,而那些确实成为淋巴细胞的细胞正常表达Tac。这些结果表明,艾滋病患者的成母反应较差与okt10、HLA-DR和Tac在刺激后未能增加有关。
Surface marker expression on peripheral blood mononuclear cells (PBMC) was evaluated daily in PHA- and PWM-stimulated cultures of eight AIDS patients and eight normals. Before culture, the patients' cells showed the characteristic decrease in OKT 4+ cells (normals 40.4%, patients 22.3%; P<0.001), increase in OKT 8+ cells (normals 27.6%, AIDS 38.4%; P=0.002), increase in OKT 10+ cells (normals 15.5%, AIDS 42.8%; P=0.002), and increase in HLA-DR+ cells (normals 11.4%, AIDS 28.7%; P=0.01). The percentage of OKT 11+ cells remained unchanged, while the percentage of OKT 3+ cells dropped over the first 2 days in PHA but not in PWM cultures of both groups (PHA: normals 69.8% to 35.1%; P=0.001, AIDS 56.5 to 38.5%; P=0.001, PWM: normals 62.8%–65.9%, AIDS 66.8% to 63.9%), and recovered in both groups by day 5. In PWM cultures OKT 3+ cells increased significantly in normals but not in AIDS (normals 62.6%–77.7%; P=0.04, AIDS 61.8 to 48.7%). OKT 4 expression decreased in normal PHA cultures after 1 day (38.9% to 29.6%; P=0.05) and then recovered by day 5. Its expression increased in AIDS PHA cultures by day 5 (18.0%–41.1%; P<0.001). The final percentage of OKT 4+ cells in AIDS cultures was within the normal range (35.0%–49.0%). OKT 8 expression increased in both study groups after PHA stimulation (normals 29.5%–50.4%; P=0.002, AIDS 37.4%–50.7%; P=0.02) and in normals but not AIDS after PWM stimulation (normals 28.9%–35.5%; P=0.004, AIDS 38.5%–35.6%). Because of the relative changes in expression of OKT 4 and OKT 8, the 4/8 ratio declined in the normal PHA cultures (1.89 to 1.03; P=0.1) and increased in the AIDS cultures (0.68–1.18; P=0.09). Also, the sum of OKT 4+ and OKT 8+ cells in PHA cultures increased from 68% to 94% whist expression of OKT 11 remained unchanged, indicating co-expression of these antigens on individual cells. Both PHA- and PWM-stimulated normal cells showed an increase in OKT 10 (PHA 16.0%–53.4%; P=0.01, PWM 16.1%–33.9%; P=0.03) and HLA-DR (PHA 8.6%–27.3%; P=0.03, PWM 12.5%–26.6%; P=0.07). In AIDS PHA cultures this did not change, and in their PWM cultures OKT 10 expression declined (44.8 to 23.0%; P=0.05). The PHA- and PWM-stimulated cultures of AIDS patients showed a marked deficit in generation of Tac (PHA increased from 5.4% to 77.1% in normals and from 3.2% to 48.0% in AIDS; P=0.001; PWM increased from 6.1% to 35.3% in normals, and from 5.0% to 15.5% in AIDS; P=0.04). Analysis showed that this deficit was limited to a reduced expression on small lymphocytes and that those cells that did become lymphoblasts expressed Tac normally. These results indicate that the poor blastogenic responses in AIDS are related to failure of OKT 10, HLA-DR, and Tac to increase after stimulation.