Yamane K, Kono I, Kabashima T, Sakurai T, Kashiwagi H
Int Arch Allergy Appl Immunol. 1986;80(2):132-8. doi: 10.1159/000234041.
We investigated monocyte-mediated suppression of T lymphocyte blastogenesis in normals and patients with systemic lupus erythematosus (SLE). When monocytes from normals were cocultured with autologous T lymphocytes with a ratio of 1:1 and stimulated with phytohemagglutinin (PHA), 3H-thymidine incorporation by T lymphocytes was suppressed. This monocyte-mediated suppression was reversed by purine nucleoside phosphorylase substrate, deoxyguanosine. In SLE patients, both monocyte-mediated suppression and its reversal by deoxyguanosine were defective. The defective function was observed both in patients with active and inactive diseases. The defective function was studied sequentially before and after change in the clinical status of patients. The defects remained unaffected regardless of the disease activity. The defects in monocyte-mediated suppression and its reversal by deoxyguanosine in SLE patients as demonstrated in our study suggest the presence of intrinsic monocyte dysfunction in SLE.
我们研究了正常人和系统性红斑狼疮（SLE）患者中单核细胞介导的T淋巴细胞增殖抑制情况。当正常单核细胞与自体T淋巴细胞以1:1比例共培养并用植物血凝素（PHA）刺激时，T淋巴细胞的3H-胸腺嘧啶核苷掺入受到抑制。这种单核细胞介导的抑制作用可被嘌呤核苷磷酸化酶底物脱氧鸟苷逆转。在SLE患者中，单核细胞介导的抑制作用及其被脱氧鸟苷逆转的功能均存在缺陷。在疾病活动期和非活动期患者中均观察到功能缺陷。在患者临床状态改变前后对功能缺陷进行了连续研究。无论疾病活动度如何，缺陷均未受影响。我们的研究中所证明的SLE患者单核细胞介导的抑制作用及其被脱氧鸟苷逆转的缺陷提示SLE中存在内在的单核细胞功能障碍。
