Klatka Maria, Grywalska Ewelina, Polak Agnieszka, Roliński Jacek
Department of Pediatric Endocrinology and Diabetology,Medical University, Lublin, Poland.
Department of Clinical Immunology and Immunotherapy, Medical University, Lublin, Poland.
Ann Agric Environ Med. 2013;20(4):884-8.
The protein product of the proto-oncogene Bcl-2 is a physiological inhibitor of programmed cell death. The results obtained in our previous researches suggest that apoptosis may be involved in the regulation of an immune response in hyperthyroidism. The most common cause of hyperthyroidism is Graves' disease. The aim of this study was evaluation of expression of Bcl-2 protein in peripheral blood T lymphocytes in hyperthyroid children due to Graves' disease (GD) before and after therapy with methimazole (MMI), in comparison with healthy controls.
Thirty-two children with newly diagnosed hyperthyreosis due to GD before and after 4-6 weeks treatment with MMI, and 20 healthy controls were included into the study. The staining with monoclonal antibodies against CD8 and Bcl-2 was performed within 2 hours after collection, and followed with flow cytometry acquisition and analysis.
Our study revealed that the expression of Bcl-2 protein in circulating CD8+ T lymphocytes of patients with hyperthyreosis was significantly lower than in healthy controls (p<0.03). The expression of Bcl-2 after 4-6 week therapy with MMI returned to normal level. The difference in Bcl-2 expression between patients after treatment and control group was insignificant.
The use of MMI in the treatment of hyperthyroidism due to GD leads to the normalization of the Bcl-2 expression on the CD8+ lymphocytes in peripheral blood. Our findings suggest that the changes in the expression of Bcl-2 on the CD8+ cells indicate the involvement of these cells and Bcl-2-regulated apoptotic pathway in the pathogenesis of GD.
原癌基因Bcl-2的蛋白质产物是程序性细胞死亡的生理抑制剂。我们之前研究获得的结果表明，细胞凋亡可能参与了甲状腺功能亢进症免疫反应的调节。甲状腺功能亢进症最常见的病因是格雷夫斯病。本研究的目的是评估格雷夫斯病（GD）所致甲状腺功能亢进症患儿在接受甲巯咪唑（MMI）治疗前后外周血T淋巴细胞中Bcl-2蛋白的表达，并与健康对照进行比较。
本研究纳入了32例新诊断为GD所致甲状腺功能亢进症的患儿，在接受MMI治疗4 - 6周前后，以及20名健康对照。采集样本后2小时内用抗CD8和Bcl-2单克隆抗体进行染色，随后进行流式细胞仪采集和分析。
我们的研究显示，甲状腺功能亢进症患者循环CD8⁺T淋巴细胞中Bcl-2蛋白的表达显著低于健康对照（p<0.03）。接受MMI治疗4 - 6周后，Bcl-2的表达恢复至正常水平。治疗后患者与对照组之间Bcl-2表达的差异不显著。
使用MMI治疗GD所致甲状腺功能亢进症可使外周血CD8⁺淋巴细胞上Bcl-2的表达恢复正常。我们的研究结果表明，CD8⁺细胞上Bcl-2表达的变化表明这些细胞及Bcl-2调节的凋亡途径参与了GD的发病机制。
