ArticleInternational journal of clinical and experimental pathology2018
NETosis may play a role in the pathogenesis of Hashimoto's thyroiditis.
Article in International journal of clinical and experimental pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Histidine alleviates Hashimoto's thyroiditis via the neutrophil extracellular traps-NF-κB signaling pathway.Scientific reports · 2026Article
- The Relationship Between Composite Inflammatory Indices and Dry Eye in Hashimoto's Disease-Induced Hypothyroid Patients.Biomedicines · 2025Article
- NETosis in hypersensitivity disorders.Molecular biology reports · 2025Review
- Melanoma-derived soluble mediators modulate neutrophil biological properties and the release of neutrophil extracellular traps.Cancer immunology, immunotherapy : CII · 2023Article
- Thyroid hormones and minerals in immunocorrection of disorders in autoimmune thyroid diseases.Frontiers in endocrinology · 2023Review
- Machine learning-based detection of immune-mediated diseases from genome-wide cell-free DNA sequencing datasets.NPJ genomic medicine · 2022Article
- Neutrophil extracellular traps and neutrophil-derived mediators as possible biomarkers in bronchial asthma.Clinical and experimental medicine · 2022Article
- Neutrophil Extracellular Traps, Angiogenesis and Cancer.Biomedicines · 2022Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutrophil extracellular traps (NETs) are shown to play important roles in the progression or development of systemic autoimmune diseases. However, implication of NETs or NETosis in the pathogenesis of non-systemic autoimmune diseases such as Hashimoto's thyroiditis (HT), a chronic inflammatory organ-specific autoimmune disease, has not been previously reported. In the present study, our results demonstrate that the concentration of NET products, neutrophil elastase (NE) and proteinase 3 (PR3) in plasma, are significantly higher in the patients with HT than in healthy controls, respectively. In addition, PR3 concentration in plasma was positively associated with the titers of autoantibodies against thyroglobulin (TGAb) and thyroid peroxidase (TPOAb) in serum, respectively. Consistently, NETosis was more markedly induced in neutrophils derived from the HT patients than controls. Concomitantly, IL-6 production in the NETosis induction system in the neutrophils from the patients was significantly higher than those in controls. Moreover, serum from HT patients but not healthy controls induced more pronounced NETosis in neutrophils. Meanwhile, our immuno-fluorescence staining results showed that NETs from the HT patients contained autoantigens. These findings together indicate roles for NETs and/or NETosis in autoantibody generation as well as pathogenesis of HT. Therefore, the underlying mechanisms of NETs in the pathogenesis of HT warrant further study.
Indexed as
Identifiers
31938139PMC6958043W3013986469What OpenQuestion holds
Registered trials
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