Abstract
Th17 and regulatory lymphocyte subsets such as Tregs and Bregs have been reported to play important roles in autoimmune diseases. The aim of this work was to perform quantitative studies of circulating Th17, Tregs, and Bregs in patients with new-onset Graves' disease (GD). Twenty GD patients and 20 healthy controls were involved in this study. Blood samples were taken for flow cytometry detection of CD4+IL-17+ Th17, CD4+Foxp3+ Tregs, and CD19+CD1dhiCD5+ Bregs and meanwhile, for real-time PCR measurement of gene expressions of RORγt, IL-17 and IL-10. The proportions of Tregs and Bregs as well as the Foxp3 gene expression but not IL-10 were significantly decreased in GD group compared with the healthy controls. The frequency of Th17 together with the gene expressions of RORγt and IL-17 were significantly increased in the GD group. Furthermore, the Th17/Treg ratio was also significantly higher in GD group. A significant positive correlation between Th17 and TSAb (r = 0.656, p < 0.001) but significant negative correlations between Treg/Breg and TSAb (r = −0.339, p = 0.032; r = −0.759, p < 0.001) were identified among the participants. This study indicated that increased Th17 and impaired Treg responses, along with a decreased number of CD19+CD1dhiCD5+ Breg cells, were involved in GD pathogenesis.
Highlights
Graves’ disease (GD) is one of the most common organspecific autoimmune diseases
No significant differences were noted in the age and gender distributions between the healthy controls and GD patients
The activity of thyroid-stimulating antibody (TSAb), the specific thyroid autoantibody produced in GD, was significantly higher in GD patients than in controls
Summary
Graves’ disease (GD) is one of the most common organspecific autoimmune diseases. It is characterized by hyperthyroidism and specific thyroid autoantibodies against thyroidstimulating hormone receptor (TSHR) and is commonly accompanied by autoantibodies against thyroglobulin (TG) and thyroid peroxidase (TPO).Despite the environmental and genetic factors, the aetiology of GD is partly due to the breakdown of immune self-tolerance to thyroid autoantigen TSHR, leading to autoreactive T and B cells. Graves’ disease (GD) is one of the most common organspecific autoimmune diseases. It is characterized by hyperthyroidism and specific thyroid autoantibodies against thyroidstimulating hormone receptor (TSHR) and is commonly accompanied by autoantibodies against thyroglobulin (TG) and thyroid peroxidase (TPO). Despite the environmental and genetic factors, the aetiology of GD is partly due to the breakdown of immune self-tolerance to thyroid autoantigen TSHR, leading to autoreactive T and B cells. It has been widely accepted that the exaggerated T helper (Th) 2 response plays a pivotal role in GD development [1,2,3]. The Th2 theory cannot explain all conditions. Researchers have recognized that two other CD4+ T cell subsets and one B cell subtype, namely, the Th17 and regulatory T (Treg) cells, along with regulatory B (Breg) cells, may participate in GD pathogenesis [4,5,6,7,8,9]
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