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骨髓在实验性格雷夫斯病和甲状腺眼病中的潜在参与

Anne Gulbins¹, Mareike Horstmann¹, Simone Keitsch²

¹Molecular Ophthalmology, Department of Ophthalmology, University Hospital Essen, University Duisburg-Essen, Essen, Germany.

Frontiers in endocrinology

|October 9, 2023

概括

格雷夫斯病和甲状腺眼病激活骨髓免疫细胞. 用林西替尼布阻断IGF-1R通过升高调节阿尔金酶-1来阻止这种激活,从而抑制免疫反应.

科学领域:

免疫学免疫学免疫学
内分泌学在内分泌学.
眼科医生眼科眼科

背景情况:

格雷夫斯病是一种针对甲状腺刺激激素受体 (TSHR) 的自身免疫性疾病.
甲状腺眼病 (TED) 是一个常见的表现,涉及TSHR与轨道纤维细胞中IGF-1R的交叉声.
骨髓在格雷夫斯病和TED病原体中的作用在很大程度上是未知的.

研究的目的:

在实验性格雷夫斯病和TED期间调查骨髓激活.
为了确定干扰IGF-1R信号是否可以在这些条件下阻止骨髓激活.

主要方法:

通过TSHR免疫接种在小鼠中诱导实验性格雷夫斯病.
用林西替尼治疗,林西替尼是一种IGF-1R抗剂.
对免疫细胞种群,造血干细胞,细胞因子概况和骨髓中阿基因酶-1表达的分析.

主要成果:

TSHR免疫增加了骨髓中的T淋巴细胞,B淋巴细胞,造血干细胞和促炎细胞因子.
林西替尼治疗使T淋巴细胞数量正常化,防止GR1阳性细胞减少,并阻止干细胞和促炎媒介体的增加.
林西替尼提升了骨髓的阿基因酶-1的调节,导致阿基因的耗尽和免疫抑制,这种情况通过阿基因的复制而逆转.

结论:

骨髓激活发生在实验性格雷夫斯病和TED中.
在这个模型中,林西尼尼有效地阻止了骨髓激活.
林西尼布介导的免疫抑制部分是由于阿基因酶-1的上调和阿基因的消耗.

关键词:

这是自身免疫力.骨髓骨髓骨髓骨髓骨髓这是一种炎症炎症炎症炎症.林西尼尼比 (linsitinib) 是一种小分子IGF-1R抗剂GD:格雷夫斯病甲状腺眼睛疾病 (TED)

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