Wang Shuo, Liu Yongping, Zhao Na, Cui Xuejiao, Huang Mingshi, Li Yushu, Shan Zhongyan, Teng Weiping
Liaoning Provincial Key Laboratory of Endocrine Diseases, Department of Endocrinology and Metabolism, Institute of Endocrinology, The First Affiliated Hospital of China Medical University, Shenyang, China.
Front Endocrinol (Lausanne). 2018 Oct 23;9:629. doi: 10.3389/fendo.2018.00629. eCollection 2018.
Hashimoto's thyroiditis (HT) is a common autoimmune disease accompanied by lymphocyte infiltration and thyroid tissue destruction. IL-34 was first described in 2008, and its involvement in the development of many autoimmune diseases has been recently identified. However, whether IL-34 is a regulatory factor in HT is unclear. Here, we demonstrate that IL-34 is expressed on thyroid follicular epithelial cells and that IL-34 expression is significantly reduced in thyroid tissue in patients with HT and spontaneous autoimmune thyroiditis (SAT) models. Serum IL-34 levels in patients with HT are also significantly reduced. In addition, IL-34 is associated with thyroid autoantibodies in both thyroid tissue and serum. Furthermore, our data show that IL-34 participates in the apoptosis resistance of thyrocytes in HT induced by CSF-1R and may be a potential indicator for evaluating thyrocyte damage.
桥本甲状腺炎（HT）是一种常见的自身免疫性疾病，伴有淋巴细胞浸润和甲状腺组织破坏。白细胞介素-34（IL-34）于2008年首次被描述，最近已确定其参与多种自身免疫性疾病的发展。然而，IL-34是否为HT中的调节因子尚不清楚。在此，我们证明IL-34在甲状腺滤泡上皮细胞上表达，且在HT患者及自发性自身免疫性甲状腺炎（SAT）模型的甲状腺组织中，IL-34表达显著降低。HT患者的血清IL-34水平也显著降低。此外，IL-34在甲状腺组织和血清中均与甲状腺自身抗体相关。此外，我们的数据表明，IL-34参与了CSF-1R诱导的HT中甲状腺细胞的抗凋亡过程，可能是评估甲状腺细胞损伤的一个潜在指标。
