ArticleEndocrine2016
Impaired immune regulation after radioiodine therapy for Graves' disease and the protective effect of Methimazole.
Article in Endocrine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Effect of methimazole treatment on Th1, Th17, and Th22 lymphocytes in pediatric Graves' disease patients.Frontiers in immunology · 2024Article
- [The features of regulatory T-blood cells subpopulation and the level of CD25 expression in patients with Graves' disease in dynamics after radioactive iodine therapy].Problemy endokrinologii · 2023Article
- Regulatory B Cells Involvement in Autoimmune Phenomena Occurring in Pediatric Graves' Disease Patients.International journal of molecular sciences · 2021Article
- The longer the antithyroid drug is used, the lower the relapse rate in Graves' disease: a retrospective multicenter cohort study in Korea.Endocrine · 2021Article
- Percentage and function of CD4+CD25+ regulatory T cells in patients with hyperthyroidism.Molecular medicine reports · 2018Article
- Limited cutaneous systemic sclerosis arising in a patient with Graves' disease.BMJ case reports · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Both therapies for Graves' disease (GD), radioactive iodine (RAI) and antithyroid drugs (ATD), were reported to have specific immune effects. We aimed at investigating the effects of RAI therapy on cellular subsets involved in immune regulation. We conducted a thirty day follow-up prospective cohort study of adult patients. Patients eligible for RAI therapy at our centre were approached. Twenty seven patients with GD were recruited, among whom 11 were treated with ATD. Twenty-two healthy subjects (HS) were also studied. Over time, frequency of regulatory T cells (Treg) and of invariant natural killer T cells (iNKT), along with Treg cell-mediated suppression and underlying mechanisms, were monitored in the peripheral blood. Variance in frequency of Treg and iNKT after RAI therapy was higher in GD patients than in HS over time (p < 0.0001). Reduced Treg suppressive function was observed after RAI therapy in GD patients (p = 0.002). ATD medication prior to RAI dampened these outcomes: less variation of Treg frequency (p = 0.0394), a trend toward less impaired Treg function, and prevention of reduced levels of suppressive cytokines (p < 0.05). Shortly after RAI therapy, alterations in immunoregulatory cells in patients with GD were observed and partially prevented by an ATD pretreatment. Worsening of autoimmunity after RAI was explained in previous studies by enhanced immune activity. This study adds new highlights on immune regulation deficiencies after therapeutic interventions in thyroid autoimmunity.
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