Abstract
Graves’s disease is the most common type of autoimmune hyperthyroidism. Numerous studies indicate different factors contributing to the onset of the disease. Despite years of research, the exact pathomechanism of Graves’ disease still remains unresolved, especially in the context of immune response. B cells can play a dual role in autoimmune reactions, on the one hand, as a source of autoantibody mainly targeted in the thyroid hormone receptor (TSHR) and, on the other, by suppressing the activity of proinflammatory cells (as regulatory B cells). To date, data on the contribution of Bregs in Graves’ pathomechanism, especially in children, are scarce. Here, we investigated the frequencies of Bregs before and during a methimazole therapy approach. We reported higher Foxp3+ and IL-10+ Breg levels with CD38- phenotype and reduced numbers of CD38 + Foxp3 + IL-10+ in pediatric Graves’ patients. In addition, selected Breg subsets were found to correlate with TSH and TRAb levels significantly. Noteworthy, certain subpopulations of Bregs were demonstrated as prognostic factors for methimazole therapy outcome. Our data demonstrate the crucial role of Bregs and their potential use as a biomarker in Graves’ disease management.
Highlights
A decline in the level of B cells with immunosuppressive phenotype was demonstrated within CD19+CD38+ population with co-expression of both IL-10 and Foxp3
We found that a group with high CD38+Foxp3+IL-10+ cell numbers demonstrated the most significant increase in TSH level after 1–2 years of MMI treatment
Despite the lack of essential differences at the beginning of treatment, we found that patients with higher numbers of CD38+Foxp3+ and CD38+Foxp3+IL-10+ Bregs demonstrated higher TSH levels achieved with methimazole use compared to subjects with low numbers of these subpopulations
Summary
Considering our own observations, these numbers seem relevant, even in the context of pediatric patients [2,3]
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