IL-34 Expression Is Reduced in Hashimoto's Thyroiditis and Associated With Thyrocyte Apoptosis.
IL-34 Expression Is Reduced in Hashimoto's Thyroiditis and Associated With Thyrocyte Apoptosis.
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桥本甲状腺炎中 IL-34 表达减少并与甲状腺细胞凋亡相关
DOI：
10.3389/fendo.2018.00629
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发表时间：
2018
影响因子：
5.2
通讯作者：
Teng W
中科院分区：
文献类型：
--
作者：
Wang S;Liu Y;Zhao N;Cui X;Huang M;Li Y;Shan Z;Teng W
桥本甲状腺炎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。IL-34于2008年首次被描述，最近发现其参与许多自身免疫性疾病的发展。然而，IL-34是否是HT的调节因子尚不清楚。在这里，我们证明IL-34在甲状腺滤泡上皮细胞上表达，并且在HT和自发性自身免疫性甲状腺炎（SAT）模型患者的甲状腺组织中IL-34的表达显著降低。HT患者血清IL-34水平也显著降低。此外，IL-34与甲状腺组织和血清中的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中甲状腺细胞的凋亡抵抗，可能是评估甲状腺细胞损伤的潜在指标。
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.
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过量碘通过诱导自噬抑制促进甲状腺滤泡上皮细胞凋亡，并与桥本甲状腺炎相关
影响因子：
12.8
作者：
Xu, Chengcheng;Wu, Fei;Xiao, Yichuan
通讯作者：
Xiao, Yichuan
DOI：
10.1042/cs20150176
发表时间：
2015-08
期刊：
Clinical science (London, England : 1979)
影响因子：
--
作者：
Zwicker S;Martinez GL;Bosma M;Gerling M;Clark R;Majster M;Söderman J;Almer S;Boström EA
通讯作者：
Boström EA
影响因子：
7.3
作者：
Baud'Huin, Marc;Renault, Romain;Heymann, Dominique
通讯作者：
Heymann, Dominique
影响因子：
56.9
作者：
Lin, Haishan;Lee, Ernestine;Williams, Lewis T.
通讯作者：
Williams, Lewis T.
影响因子：
5.8
作者：
CHIOVATO, L;BASSI, P;PINCHERA, A
通讯作者：
PINCHERA, A