ArticlePloS one2015
Characterization of Regulatory B Cells in Graves' Disease and Hashimoto's Thyroiditis.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- Pooled it
- Article
- Regulatory B Cells in Systemic Sclerosis Isolated or Concomitant With Hashimoto Thyroiditis.Frontiers in immunology · 2022Article
- Simulation Model for Hashimoto Autoimmune Thyroiditis Disease.Endocrinology · 2021Article
- Checkpoint Receptor TIGIT Expressed on Tim-1Cell reports · 2020Article
- Mass Cytometry Studies of Patients With Autoimmune Endocrine Diseases Reveal Distinct Disease-Specific Alterations in Immune Cell Subsets.Frontiers in immunology · 2020Article
- Molecular Insights Into the Relationship Between Autoimmune Thyroid Diseases and Breast Cancer: A Critical Perspective on Autoimmunity and ER Stress.Frontiers in immunology · 2019Review
- Role of the T and B lymphocytes in pathogenesis of autoimmune thyroid diseases.Thyroid research · 2018Article
- Frequency of IL-10-producing regulatory B cells associated with disease activity in thyroid-associated orbitopathy.International journal of ophthalmology · 2018Article
- Breg Cells in Celiac Disease Isolated or Associated to Hashimoto's Thyroiditis.International journal of endocrinology · 2018Article
- Pathogenic Th17 and Th22 cells are increased in patients with autoimmune thyroid disorders.Endocrine · 2017Article
- TIM-1 defines a human regulatory B cell population that is altered in frequency and function in systemic sclerosis patients.Arthritis research & therapy · 2017Article
- Increased Circulating Th17 but Decreased CD4BioMed research international · 2017Article
- Article
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
A hallmark of regulatory B cells is IL-10 production, hence their designation as IL-10+ B cells. Little is known about the ability of self-antigens to induce IL-10+ B cells in Graves' disease (GD), Hashimoto's thyroiditis (HT), or other autoimmune disease. Here we pulsed purified B cells from 12 HT patients, 12 GD patients, and 12 healthy donors with the thyroid self-antigen, thyroglobulin (TG) and added the B cells back to the remaining peripheral blood mononuclear cells (PBMCs). This procedure induced IL-10+ B-cell differentiation in GD. A similar tendency was observed in healthy donors, but not in cells from patients with HT. In GD, B cells primed with TG induced IL-10-producing CD4+ T cells. To assess the maximal frequency of inducible IL-10+ B cells in the three donor groups PBMCs were stimulated with PMA/ionomycin. The resulting IL-10+ B-cell frequency was similar in the three groups and correlated with free T3 levels in GD patients. IL-10+ B cells from both patient groups displayed CD25 or TIM-1 more frequently than did those from healthy donors. B-cell expression of two surface marker combinations previously associated with regulatory B-cell functions, CD24hiCD38hi and CD27+CD43+, did not differ between patients and healthy donors. In conclusion, our findings indicate that autoimmune thyroiditis is not associated with reduced frequency of IL-10+ B cells. These results do not rule out regulatory B-cell dysfunction, however. The observed phenotypic differences between IL-10+ B cells from patients and healthy donors are discussed.
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