ArticleJournal of endocrinological investigation2024
Notch signaling regulates Th17 cells differentiation through PI3K/AKT/mTORC1 pathway and involves in the thyroid injury of autoimmune thyroiditis.
Article in Journal of endocrinological investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Role of interleukin 17 and T helper cells 17 cells as a new immune target and signalling in the pathogenesis and treatment of autoimmune thyroid diseases.Annals of medicine · 2025Pooled it
- Synergistic role of molecular imaging and genomics in thyroid cancer management: from diagnosis to personalized treatment.Journal of translational medicine · 2026Review
- γ-Secretase inhibitor ameliorates thyroid autoimmune damage via blocking Notch1 signaling and reducing γδT17 cells in EAT mice.Endocrine journal · 2026Article
- Targeting METTL3 Attenuates Thyroid Inflammatory Injury by Restoring Th17/Treg Balance through a YTHDC2-m6A-Dependent KDR/VEGFA Loop.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Metabolic reprogramming of Th17/Treg imbalance in autoimmune thyroid diseases.Cell communication and signaling : CCS · 2026Review
- Th17/Treg cell imbalance in allergic rhinitis: mechanisms and therapeutic implications.Genes and immunity · 2026Review
- Network pharmacological and experimental validation of the mechanism of Chaihu Guizhi Ganjiang decoction regulating T helper cell 17/regulatory T cell balance to improve autoimmune hepatitis.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2026Article
- HMGB1 dysregulation: a neuroimmune bridge to cognitive impairment in autoimmune thyroiditis.Frontiers in immunology · 2026Article
- Buzhong Yiqi Decoction Regulates Th17 Cells Differentiation in Autoimmune Thyroiditis through PTEN/AKT-immunometabolism Axis.Endocrine, metabolic & immune disorders drug targets · 2026Article
- HE4: a potential diagnostic biomarker in autoimmune diseases.Central-European journal of immunology · 2026Review
- TIGIT/SHIP-1/RelB regulating Th1 inflammation in smoking induced COPD.Respiratory research · 2025Article
- Adiponectin pathway regulates cerebral metabolic dysfunction and neuroinflammation via the AdipoR1/PI3K/Akt axis in Perioperative Neurocognitive Disorder.BMC geriatrics · 2025Article
- Muscone Attenuates Uveitis Through the PI3K/AKT Signaling Pathway.Investigative ophthalmology & visual science · 2025Article
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7 authors.
Funding
Abstract
purposeAutoimmune Thyroiditis (AIT) is the most common thyroid disease; however, there were no measures to prevent the progression of the disease. The present study attempts to identify that Notch signaling regulates the differentiation of T helper 17 (Th17) cells by activating downstream Phosphatidylinositol-3 kinase/protein kinase/mechanistic target of rapamycin complex 1 (PI3K/AKT/mTORC1) pathway participating in the thyroid injury of the experimental autoimmune thyroiditis (EAT).
methodsIn vivo experiments, mice were randomly divided into 4 groups: a control group, an EAT group, and two groups with LY294002 treatment (pTg plus 25 mg/kg or 50 mg/kg LY294002, respectively). The degrees of thyroiditis were evaluated, and the percentage of Th17 cells, expression of interleukin-17A (IL-17A), and the main components of the Notch-PI3K signaling pathway were detected in different groups. In vitro experiments, two different dosages of LY294002 (25 and 50 μM) were used to intervene splenic mononuclear cells (SMCs) from EAT mice to further evaluate the regulatory effect of Notch-PI3K pathway on Th17 cells.
resultsOur data demonstrate that the infiltration of Th17 cells and the expressions of IL-17A, Notch, hairy and split 1 (Hes1), p‑AKT (Ser473), p‑AKT (Thr308), p‑mTOR (Ser2448), S6K1, and S6K2 increased remarkably in EAT mice. After PI3K pathway was blocked, the degrees of thyroiditis were significantly alleviated, and the proportion of Th17 cells, the expression of IL-17A, and the above Notch-PI3K pathway-related molecules decreased in a dose-dependent manner. Additionally, the proportion of Th17 cells was positively correlated with the concentration of serum thyroglobulin antibody (TgAb), IL-17A, and Notch-PI3K pathway-related molecules mRNA levels.
conclusionsNotch signal promotes the secretion of IL-17A from Th17 cells by regulating the downstream PI3K/AKT/mTORC1 pathway through Hes-Phosphatase and tensin homolog (PTEN) and participates in thyroid autoimmune damage, and the PI3K pathway inhibitor may play important effects on AIT by affecting Th17 cells differentiation.
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