Background: Interrelation between thyrocytes and immunocytes has been established. However, the roles of mast cells and thyroid hormones in the triggering mechanism of thyroid autoimmune processes have been insufficiently investigated. This study evaluated the role of thyroid hormones and mast cells in the mechanisms of losing tolerance to thyroid autoantigens. Materials and Methods: Two groups of patients were studied: patients with Graves’ disease and patients with nodular euthyroid goiter. Wistar rats with induced exogenous hypothyroidism, thyrotoxicosis, and thyrotoxicosis in parallel with administration of interleukin-2 were used. The levels of hormones, autoantibodies, and cytokines in the serum and thyroid tissue were analyzed through the enzyme-linked immunosorbent assay. Morphological verification was performed through the immune-histochemical method with antibodies against tryptase and CD86. Transmission electron microscopy and laser confocal microscopy were used. Results: In both Graves’ disease and induced thyrotoxicosis, we detected a significant increase in the levels of interferon-γ, active interfollicular infiltration and degranulation of mast cells, and the intrathyroid overexpression of CD86. Complex analysis of the rat’s thyroid morphofunctional state and systemic and local levels of cytokines in induced thyrotoxicosis and hypothyroidism demonstrated an increase of intrathyroid degranulation of mast cells and a drastic disruption of IFNγ/IL10 balance. Conclusions: When exposed to excessive amounts of thyroid hormones, an inflammatory response is triggered in the thyroid gland, and mast cells overexpress costimulating CD86 in the thyroid. This finding confirms their possible involvement in auto­antigen presentation. Significant increase in the levels of interferon-γ shows a determining influence of cytokine on the progression of the pathological process.
Int Arch Allergy Immunol

中文翻译：

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甲状腺激素，肥大细胞和炎症介质在自身免疫性甲状腺疾病的发生和发展中的作用。

背景：甲状腺细胞和免疫细胞之间的相互关系已经建立。然而，尚未充分研究肥大细胞和甲状腺激素在甲状腺自身免疫过程触发机制中的作用。这项研究评估了甲状腺激素和肥大细胞在失去对甲状腺自身抗原的耐受性的机制中的作用。材料和方法：研究了两组患者：Graves病患者和结节性甲状腺甲状腺肿患者。使用与白细胞介素2给药同时诱导外源性甲状腺功能减退，甲状腺毒症和甲状腺毒症的Wistar大鼠。通过酶联免疫吸附法分析血清和甲状腺组织中激素，自身抗体和细胞因子的水平。通过免疫组织化学方法用针对类胰蛋白酶和CD86的抗体进行形态学验证。使用透射电子显微镜和激光共聚焦显微镜。结果：在Graves病和诱发的甲状腺毒症中，我们都检测到干扰素-γ的水平，肥大细胞的活跃的小孔间浸润和脱粒以及CD86的甲状腺内过表达均显着增加。对大鼠甲状腺形态功能状态以及诱发的甲状腺毒症和甲状腺功能减退症中系统和局部细胞因子水平的复杂分析表明，甲状腺内肥大细胞脱颗粒增加，IFNγ/ IL10平衡急剧破坏。结论：当暴露于过量的甲状腺激素时，会在甲状腺中引发炎症反应，肥大细胞会在甲状腺中过表达共刺激CD86。这一发现证实了他们可能参与了自身抗原的呈递。干扰素-γ水平的显着增加表明细胞因子对病理过程的发展具有决定性的影响。
Int Arch过敏免疫