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缺口信号通过PI3K/AKT/mTORC1通路调节Th17细胞的分化,并涉及到自身免疫性甲状腺炎的甲状腺损伤

C He1, Y Li1, L Gan1

  • 1Department of Endocrinology and Metabolism, Binzhou Medical University Hospital, Binzhou, 256600, People's Republic of China.

Journal of endocrinological investigation
|January 29, 2024
PubMed
概括

突信号驱动自身免疫性甲状腺炎,通过通过PI3K/AKT/mTORC1通路促进T辅助17细胞的分化. 抑制这种途径可以缓解甲状腺损伤,这表明自身免疫甲状腺炎的治疗点.

关键词:
自免疫性甲状腺炎的发生.在LY294002中使用.口信号传输是没有的.在PI3K/AKT/mTORC1路径中.在Th17细胞中.

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