Decreased β-catenin expression contributes to IFNγ-induced chemokine secretion and lymphocyte infiltration in Hashimoto's thyroiditis.
Fei WuChaoming MaoXiao MouChengcheng XuTingting ZhengLing BuXuan LuoQingyan LuXuefeng WangPublished in: Endocrine connections (2022)
Hashimoto's thyroiditis (HT) is a very common organ-specific autoimmune disease characterized by lymphocyte infiltration and the destruction of thyroid follicular cells (TFCs), in which IFN-γ and chemokines play pivotal roles. Moreover, β-catenin has been implicated in the regulation of T cell infiltration. However, whether β-catenin is involved in Hashimoto's thyroiditis is unknown. Here, we examined β-catenin expression in thyroid tissues and investigated its role in the pathogenesis of HT. The results showed that β-catenin expression was markedly reduced in the thyroid tissues of HT patients; more importantly, IFN-γ treatment markedly reduced the expression of β-catenin and was accompanied by the secretion of chemokines such as CCL5, CXCL16, GRO-β, and GRO-γ in TFCs in vitro, which was attributed to GSK-3β/β-catenin signaling pathway activation. Collectively, the decreased expression of β-catenin might contribute to IFNγ-induced chemokine secretion and lymphocyte infiltration in the development of HT.
Keyphrases
- poor prognosis
- epithelial mesenchymal transition
- cell proliferation
- immune response
- dendritic cells
- end stage renal disease
- binding protein
- gene expression
- long non coding rna
- multiple sclerosis
- chronic kidney disease
- induced apoptosis
- peripheral blood
- high glucose
- signaling pathway
- peritoneal dialysis
- oxidative stress
- ejection fraction
- cell death
- diabetic rats
- endothelial cells
- mass spectrometry
- cell cycle arrest
- patient reported outcomes
- endoplasmic reticulum stress