ArticleJournal of autoimmunity2018
Activation of thyroid antigen-reactive B cells in recent onset autoimmune thyroid disease patients.
Article in Journal of autoimmunity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 2 of them syntheses that pooled it.
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.
The trial behind it
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Who cites it
34 citing papers in PubMed, 2 syntheses or guidelines pooled it, 47 citations in OpenAlex.
- Autoimmune thyroiditis and comorbid autoimmune diseases: global research landscape and future directions.Frontiers in immunology · 2026Pooled it
- Immune Checkpoint Inhibitors-Related Thyroid Dysfunction: Epidemiology, Clinical Presentation, Possible Pathogenesis, and Management.Frontiers in endocrinology · 2021Pooled it
- Activation of Anergic B Cells During Development of Autoimmunity.Immunological reviews · 2026Review
- Inverse association between peripheral natural killer cells and thyroid autoimmunity in cases of miscarriage: Evidence from a cross-sectional study.The Journal of international medical research · 2026Article
- Lyn governs the establishment and maintenance of B cell anergy by suppressing PI3K signaling.Nature communications · 2026Article
- A reliable and explainable deep learning framework for clinical-grade endocrine disorder risk prediction and decision support.Frontiers in artificial intelligence · 2026Article
- Case Report: longitudinal immunoglobulin abnormalities preceding IgA-λ MGUS and colonic DLBCL: a case suggesting immune-driven B-cell dysregulation.Frontiers in oncology · 2026Article
- Deletion of Ptpn2 in B cells promotes autoimmunity via TLR and JAK/STAT signaling.JCI insight · 2025Article
- Hub genes and key pathways of Graves' disease: bioinformatics analysis and validation.Hormones (Athens, Greece) · 2025Article
- Genetic and Plasma Proteomic Approaches to Identify Therapeutic Targets for Graves' Disease and Graves' Ophthalmopathy.ImmunoTargets and therapy · 2025Article
- The Role of the Immune System in the Course of Hashimoto's Thyroiditis: The Current State of Knowledge.International journal of molecular sciences · 2024Review
- IgDPathogens (Basel, Switzerland) · 2024Article
- The serum concentration and activity of DPP4 is positively related with the severity of hyperthyroidism in patients with Graves' disease.Annals of medicine · 2023Article
- Expansion of extrafollicular B and T cell subsets in childhood-onset systemic lupus erythematosus.Frontiers in immunology · 2023Article
- Selective Silencing of Disease-Associated B Lymphocytes from Hashimoto's Thyroiditis Patients by Chimeric Protein Molecules.International journal of molecular sciences · 2022Article
- High levels of thyroid hormones promote recurrence of Graves' disease via overexpression of B-cell-activating factor.Journal of clinical laboratory analysis · 2022Article
- SARS-CoV-2 infection relaxes peripheral B cell tolerance.The Journal of experimental medicine · 2022Article
- Role of inhibitory signaling in peripheral B cell tolerance.Immunological reviews · 2022Review
- Peripheral immunophenotyping of AITD subjects reveals alterations in immune cells in pediatric vs adult-onset AITD.iScience · 2022Article
- CD11cFrontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Autoimmune thyroid disease (AITD), including Hashimoto's thyroiditis (HT) and Graves' disease (GD), is the most common autoimmune disorder in the United States, affecting over 20 million people. At the time of diagnosis, both HD and GD are characterized by the accumulation of B and T lymphocytes in the thyroid gland and production of autoantibodies targeting the thyroid, indicating that a breach in tolerance of autoreactive lymphocytes has occurred. However, few studies have sought to understand the underlying pathogenesis of AITD that ultimately leads to production of autoantibodies and loss of thyroid function. In this study, we analyzed the phenotype of thyroid antigen-reactive B cells in the peripheral blood of recent onset and long standing AITD patients. We found that in recent onset patients thyroid antigen-reactive B cells in blood no longer appear anergic, rather they express CD86, a marker of activation. This likely reflects activation of these cells leading to their production of autoantibodies. Hence, this study reports the early loss of anergy in thyroid antigen-reactive B cells, an event that contributes to development of AITD.
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Registered trials
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.