ArticleThe Journal of clinical endocrinology and metabolism2018
Interferon-α Triggers Autoimmune Thyroid Diseases via Lysosomal-Dependent Degradation of Thyroglobulin.
Article in The Journal of clinical endocrinology and metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 35 citations in OpenAlex.
- Cell-intrinsic functions of PD-L1 activate autophagy and prevent cytokine-induced apoptosis.Science advances · 2026Article
- Article
- Endoplasmic reticulum stress in Hashimoto's thyroiditis: a candidate amplification node linking thyroid-specific vulnerability and immune dysregulation.Frontiers in immunology · 2026Review
- Endoplasmic reticulum stress and unfolded protein response in immune cell function.Frontiers in immunology · 2025Review
- The Impact of Environmental Factors on the Development of Autoimmune Thyroiditis-Review.Biomedicines · 2024Review
- The role of autophagy in Graves disease: knowns and unknowns.Frontiers in cell and developmental biology · 2024Review
- Genetics and epigenetics of autoimmune thyroid diseases: Translational implications.Best practice & research. Clinical endocrinology & metabolism · 2023Review
- Thyroid function and associated mood changes after COVID-19 vaccines in patients with Hashimoto thyroiditis.Frontiers in immunology · 2023Article
- ER-phagy: mechanisms, regulation, and diseases connected to the lysosomal clearance of the endoplasmic reticulum.Physiological reviews · 2022Review
- Microarray profiling and functional analysis reveal the regulatory role of differentially expressed plasma circular RNAs in Hashimoto's thyroiditis.Immunologic research · 2022Article
- Identification of New Rare Variants Associated With Familial Autoimmune Thyroid Diseases by Deep Sequencing of Linked Loci.The Journal of clinical endocrinology and metabolism · 2021Article
- An update on the pathogenesis of Hashimoto's thyroiditis.Journal of endocrinological investigation · 2021Review
- HLA Class I Upregulation and Antiviral Immune Responses in Graves Disease.The Journal of clinical endocrinology and metabolism · 2021Article
- Bioinformatics analysis of key genes and pathways in Hashimoto thyroiditis tissues.Bioscience reports · 2020Article
- Graves' disease.Nature reviews. Disease primers · 2020Review
- Whole-genome genotyping and resequencing reveal the association of a deletion in the complex interferon alpha gene cluster with hypothyroidism in dogs.BMC genomics · 2020Article
- Hepatitis C Virus Infection of Human Thyrocytes: Metabolic, Hormonal, and Immunological Implications.The Journal of clinical endocrinology and metabolism · 2020Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Context: Autoimmune thyroid diseases (AITDs) arise from complex interactions among genetic, epigenetic, and environmental factors. Thyroglobulin (TG) is a major susceptibility gene for both Graves disease and Hashimoto thyroiditis. Interferon-α (IFNα), a cytokine secreted during viral infections, has emerged as a key trigger of AITD. We have shown that IFNα upregulates TG transcription; however, how the upregulation of TG transcription by IFNα triggers AITD is still unknown. Objective: To evaluate how IFNα triggers AITD by testing its effects on TG processing. Design: We exposed human thyroid cells to IFNα and evaluated its effects on TG expression and processing. Results: Human thyroid cells exposed to INFα had increased levels of TG mRNA but reduced TG protein levels, indicating TG protein degradation. IFNα induced endoplasmic reticulum stress, but surprisingly, neither the use of chemical chaperones nor proteasome inhibitor prevented IFNα-induced TG degradation. IFNα also increased LysoTracker staining and autophagy flux measured by net light chain 3 (LC3)-II and p62 fluxes. In addition, expression of autophagy markers LC3 and autophagy-related gene 5 was higher in thyroid tissues from patients with AITD. Finally, blocking lysosomal degradation prevented IFNα-induced degradation of TG. Conclusion: We have shown in this study IFNα-induced lysosomal-dependent degradation of TG in human thyroid cells. Our findings suggest that during viral infections, local thyroidal IFNα production can lead to lysosomal TG degradation, releasing pathogenic TG peptides that can trigger AITD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.