ELEVATED ADENOSINE-DEAMINASE AND PURINE NUCLEOSIDE PHOSPHORYLASE-ACTIVITY IN PERIPHERAL-BLOOD NULL LYMPHOCYTES FROM PATIENTS WITH ACQUIRED IMMUNE-DEFICIENCY SYNDROME

ELEVATED ADENOSINE-DEAMINASE AND PURINE NUCLEOSIDE PHOSPHORYLASE-ACTIVITY IN PERIPHERAL-BLOOD NULL LYMPHOCYTES FROM PATIENTS WITH ACQUIRED IMMUNE-DEFICIENCY SYNDROME
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DOI:
10.1182/blood.v65.6.1318.bloodjournal6561318
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发表时间:
1985-01-01
期刊:
影响因子:
20.3
通讯作者:
HERSH, EM
HERSH, EM
中科院分区:
医学1区
文献类型:
--
作者:
MURRAY, JL;LOFTIN, KC;HERSH, EM

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嘌呤代谢酶腺苷脱氨酶(ADA)和嘌呤核苷磷酸化酶(PNP)在淋巴细胞分化中起重要作用,这两种酶的遗传缺陷都与遗传性免疫缺陷状态有关。对16例获得性免疫缺陷综合征(AIDS)患者、7例艾滋病相关症状综合征(ARC)患者和7例无症状同性恋者外周血中ADA和PNP活性进行了检测。在艾滋病患者的零淋巴细胞中,nmo1/106淋巴细胞每小时的ADA活性显著升高(161。+-。12)与23名健康的异性恋对照组(127.+-)进行比较。8;P<0.025)。艾滋病患者的零淋巴细胞中PNP活性也显著增加(96。+-。10;P<0.005)以及来自ARC患者的(84.+-)。11:P<0.025)相对于对照组(61。+-)。5)。各组富含T细胞的细胞酶活性均无显著差异。与对照组相比,随着酶活性的升高,艾滋病患者HLADR(P<0.0025)、末端脱氧核苷酸转移酶(TdT)(P<0.0001)和花生凝集素受体(P<0.0001)阳性淋巴细胞的百分比略有增加,但差异显著。TDT阳性细胞在形态上表现为大的、核不规则的淋巴母细胞。艾滋病的细胞免疫缺陷显然不是淋巴细胞ADA或PNP活性不足的结果,而更有可能与未成熟和/或激活的淋巴细胞亚群的增加有关。
The purine metabolic enzymes adenosine deaminase (ADA) and purine nucleoside phosphorylase (PNP) are important in lymphocyte differentiation, and genetic deficiencies of either enzyme have been associated with hereditary immunodeficiency states. Both ADA and PNP activity were measured in null cell-enriched and T cell-enriched peripheral blood lymphocytes from 16 patients with the acquired immune deficiency syndrome (AIDS), 7 patients with the AIDS-related symptom complex (ARC) and 7 asymptomatic homosexuals. ADA activity in nmol/106 lymphocytes per h was significantly elevated in null lymphocytes from AIDS (161 .+-. 12) as compared with 23 healthy heterosexual controls (127 .+-. 8; P < 0.025). PNP activity was also significantly increased in null lymphocytes from AIDS patients (96 .+-. 10; P < 0.005) as well as those from ARC patients (84 .+-. 11: P < 0.025) relative to controls (61 .+-. 5). No significant differences in enzyme activity were noted in T cell-enriched cells in any group. Along with elevated enzyme activity, AIDS patients had small, yet significant, increases in the percentages of HLA-DR (P < 0.0025), terminal deoxynucleotidyl transferase (TdT) (P < 0.0001) and peanut agglutinin receptor (P < 0.0001) positive lymphocytes in the null fraction compared with controls. TdT-positive cells appeared morphologically as large lymphoblasts with irregular nuclei. The cellular immune deficiency in AIDS apparently is not a result of deficiencies in lymphocyte ADA or PNP activity, but is more likely associated with an increase in an immature and/or activated lymphocyte subset.