Starosz, A.; Stożek, K.; Moniuszko, M.; Grubczak, K.; Bossowski, A. Evaluating the Role of Circulating Dendritic Cells in Methimazole-Treated Pediatric Graves’ Disease Patients. Genes2021, 12, 164.
Starosz, A.; Stożek, K.; Moniuszko, M.; Grubczak, K.; Bossowski, A. Evaluating the Role of Circulating Dendritic Cells in Methimazole-Treated Pediatric Graves’ Disease Patients. Genes 2021, 12, 164.
Starosz, A.; Stożek, K.; Moniuszko, M.; Grubczak, K.; Bossowski, A. Evaluating the Role of Circulating Dendritic Cells in Methimazole-Treated Pediatric Graves’ Disease Patients. Genes2021, 12, 164.
Starosz, A.; Stożek, K.; Moniuszko, M.; Grubczak, K.; Bossowski, A. Evaluating the Role of Circulating Dendritic Cells in Methimazole-Treated Pediatric Graves’ Disease Patients. Genes 2021, 12, 164.
Abstract
Graves’ disease (GD) is hyperthyroidism associated with organ-specific autoimmune inflammation. GD occurs more frequently in adults than in children, however, pediatric patients are a therapeutic challenge due to cycles of remissions and relapses requiring constant monitoring at every stage of treatment administered. Dendritic cells (DCs) are considered a link between innate and adaptive immunity. DCs as antigen-presenting cells (APCs) are involved in antigen presentation to T lymphocytes, thereby, initiate shift towards effector cells. In accordance, DCs participates also in the modulation of tolerance to specific antigens. To date, the data on DC role in Graves’ pathological processes are scarce. Therefore, here we evaluated frequencies and role of circulating DCs in GD pediatric patients treated with methimazole. Flow cytometric analysis was implemented to evaluate mDC1, mDC2 and pDC cells and their correlation with clinical GD-related parameters. We found significantly higher levels of DC subsets in patients at admission. Furthermore, methimazole treatment seemed to effectively reduce subsets of DCs which, in addition, were found to differentialy correlate with thyroid function. Our study shed a new light on DCs role in pediatric GD pathomechanism. Further studies are required for mechanistic assessment of DCs exact role in disease progression and influence on thyroid function.
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