ArticleEndocrine connections2022
Decreased β-catenin expression contributes to IFNγ-induced chemokine secretion and lymphocyte infiltration in Hashimoto's thyroiditis.
Article in Endocrine connections, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- Genome-wide association study and polygenic risk prediction of hypothyroidism.Nature genetics · 2025Pooled it
- Mechanism of Buzhong Yiqi Decoction Modulates the Wnt5a/β-catenin Signaling Pathway to Ameliorate Thyroid Inflammatory Damage in Mice with Autoimmune ThyroiditisEndocrine, metabolic & immune disorders drug targets · 2026Article
- The role of CXCL16 in atherosclerosis: from mechanisms to therapy.Frontiers in immunology · 2025Review
- Expression levels of interleukin-17 and interferon-γ in peripheral blood and relationship with thyroid function in patients with Hashimoto's thyroiditis.Frontiers in molecular biosciences · 2025Article
- Deciphering the mediating role of CXCL10 in hypothyroidism-induced idiopathic pulmonary fibrosis in European ancestry: a Mendelian randomization study.Frontiers in immunology · 2024Article
- Hypothyroidism.Nature reviews. Disease primers · 2022Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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