Changes in Th1/Th2 cytokine balance in Graves' disease
Changes in Th1/Th2 cytokine balance in Graves' disease
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DOI：
10.1007/s004240000019
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发表时间：
2000-01-01
影响因子：
4.5
通讯作者：
Hojker, S
中科院分区：
文献类型：
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作者：
Kocjan, T;Wraber, B;Hojker, S
Craves病(GD)是由刺激性促甲状腺激素受体(TSHR)抗体引起的甲状腺功能亢进症。最近的研究表明，自身免疫性疾病发病机制中的一个重要因素是促进细胞免疫的Th1细胞因子和促进体液免疫的Th2细胞因子之间平衡的改变。关于GD的这种平衡转变，有相互矛盾的数据。我们的目标是确定新诊断的GD患者的Th1/Th2细胞因子平衡变化，并与健康对照组的相同平衡进行比较。我们在治疗前从健康供者和新诊断的GD患者的外周血中分离单个核细胞(MNC)。用离子霉素和佛波醇12-肉豆蔻酸酯-13-醋酸酯(PMA)联合激活MNC。培养40h后，用EL ISA法检测培养上清液中细胞因子(干扰素-γ、IL-4、IL-10、IL-12)浓度。GD患者的MNC培养产生的IL-12显著低于健康对照组，而IL-10和IL-4的产生明显高于健康对照组。GD患者MNC培养中Th1/Th2细胞因子的比值均显著低于健康对照组MNC培养中的Th1/Th2细胞因子。我们的结果表明，GD患者细胞因子的产生向Th2细胞因子反应的系统性转移，从而证实了TSHR抗体和体液免疫在GD发病机制中的关键作用。
Craves' disease (GD) is characterised by hyperthyroidism caused by stimulatory thyrotropin receptor (TSHR) antibodies. Recent research shows that an important factor in the pathogenesis of autoimmune diseases is the change in the balance between Th1 cytokines, which promote cell mediated immunity, and Th2 cytokines, which promote humoral immunity. There are contradictory data about this balance shift in GD. Our objective was to determine the Th1/Th2 cytokine balance shift in patients with newly diagnosed GD, when compared to the same balance in healthy controls. We isolated mononuclear cells (MNC) from the peripheral blood of healthy donors and from patients with newly diagnosed GD before treatment. The MNC were activated with ionomycin in combination with phorbol 12-myristate 13-acetate (PMA). After 40-hour incubation, the concentrations of the cytokines produced (IFN-gamma, IL-4, IL-10, IL-12) in the culture supernatants were measured by ELISA (Endogen, USA). The MNC cultures from patients with GD produced significantly less IL-12 and significantly more IL-10 and IL-4 than MNC cultures from healthy controls. All calculated ratios of Th1 against Th2 cytokines in MNC cultures from patients with GD were significantly lower than in MNC cultures from healthy controls. Our results show a systemic shift of cytokine production in patients with GD toward the Th2 cytokine response, thus confirming the key role of TSHR antibodies and humoral immunity in the pathogenesis of GD.