Iitaka M, Iwatani Y, Gerstein H C, Row V V, Volpé R
Endocrinology Research Laboratory, Wellesley Hospital, University of Toronto, Ontario, Canada.
Clin Endocrinol (Oxf). 1987 Sep;27(3):321-30. doi: 10.1111/j.1365-2265.1987.tb01158.x.
The monocyte procoagulant activity (PCA) production assay has been shown to be a good parameter of cell-mediated immunity. We have studied antigen-specific PCA production in peripheral blood mononuclear cells from patients with Graves' disease to determine the effect of the treatment on the cell-mediated immune response. Peripheral blood mononuclear cells from patients with untreated or relapsed Graves' disease produced significantly greater PCA with thyroid antigen stimulation than those from normal subjects. Patients both on antithyroid drugs in the hyperthyroid state and within 3 months post-131I therapy also produced significantly larger amount of PCA than normal subjects. However, there was no significant difference in PCA production with thyroid antigen stimulation between normal subjects and patients on anti-thyroid drugs in the euthyroid state, or patients over 3 months post-131I therapy. The ratio of positive to negative PCA production in patients on anti-thyroid drugs in the euthyroid state or over 3 months post-131I therapy was significantly lower than in untreated or relapsed Graves' disease patients. Mononuclear cells from patients on propylthiouracil responded to propylthiouracil in vitro by production of PCA. Cells from normal subjects, untreated Graves' disease patients, or patients with Hashimoto's thyroiditis did not produce PCA with propylthiouracil stimulation. Mononuclear cells from patients who were on propylthiouracil for more than 3 months produced greater PCA than those on the drug for less than 3 months, suggesting sensitization of lymphocytes to propylthiouracil during the course of treatment. However, after 131I therapy, they gradually became unresponsive to propylthiouracil. This study has shown that the activity of the antigen-specific response assessed by PCA production in mononuclear cells from Graves' disease patients declined after treatment, suggesting that the treatment exerted immunomodulatory effects.
单核细胞促凝活性（PCA）产生试验已被证明是细胞介导免疫的一个良好参数。我们研究了格雷夫斯病患者外周血单个核细胞中抗原特异性PCA的产生，以确定治疗对细胞介导免疫反应的影响。未经治疗或复发的格雷夫斯病患者的外周血单个核细胞在甲状腺抗原刺激下产生的PCA明显高于正常受试者。处于甲状腺功能亢进状态且正在服用抗甲状腺药物的患者以及在131I治疗后3个月内的患者产生的PCA量也明显高于正常受试者。然而，甲状腺功能正常且正在服用抗甲状腺药物的患者与正常受试者之间，或131I治疗后3个月以上的患者与正常受试者之间，在甲状腺抗原刺激下PCA的产生没有显著差异。甲状腺功能正常且正在服用抗甲状腺药物的患者或131I治疗后3个月以上的患者中，PCA产生阳性与阴性的比例明显低于未经治疗或复发的格雷夫斯病患者。服用丙硫氧嘧啶的患者的单核细胞在体外对丙硫氧嘧啶产生反应，通过产生PCA。正常受试者、未经治疗的格雷夫斯病患者或桥本甲状腺炎患者的细胞在丙硫氧嘧啶刺激下不产生PCA。服用丙硫氧嘧啶超过3个月的患者的单核细胞产生的PCA比服用该药少于3个月的患者更多，这表明在治疗过程中淋巴细胞对丙硫氧嘧啶产生了致敏作用。然而，在131I治疗后，它们逐渐对丙硫氧嘧啶无反应。这项研究表明，通过格雷夫斯病患者单核细胞中PCA产生评估的抗原特异性反应活性在治疗后下降，这表明治疗发挥了免疫调节作用。
