Abstract
T-helper (Th) 22 and Th17 cells are involved in the pathogenesis of autoimmune diseases. However, their roles in the pathogenesis of Graves’disease (GD) are unclear. This study is aimed at examining the frequency of peripheral blood Th22, Th17, and Th1 cells and the levels of plasma IL-22, IL-17, and IFN-γ in patients with GD. A total of 27 patients with new onset GD and 27 gender- and age-matched healthy controls (HC) were examined for the frequency of peripheral blood Th22, Th17, and IFN-γ cells by flow cytometry. The concentrations of plasma IL-22, IL-17, and IFN-γ were examined by enzyme-linked immunosorbent assay. The levels of serum TSHR antibodies (A-TSHR), free triiodothyronine (FT3), free thyroxine (FT4), and thyroid stimulating hormone (TSH) were examined by radioimmunoassay and chemiluminescent assay, respectively. The levels of serum TSAb were examined by enzyme-linked immunosorbent assay. In comparison with those in the HC, significantly elevated percentages of Th22 and Th17 cells, but not Th1 cells, and increased levels of plasma IL-22 and IL-17, but not IFN-γ, were detected in GD patients (P<0.0001, for both). The percentages of both Th22 and Th17 cells and the levels of plasma IL-22 and IL-17 were correlated positively with the levels of serum TSAb in GD patients (r = 0.7944, P<0.0001; r = 0.8110, P<0.0001; r = 0.7101, p<0.0001; r = 0.7407, p<0.0001, respectively). Th22 and Th17 cells may contribute to the pathogenesis of GD.
Highlights
Graves’ disease (GD) is an organ-specific autoimmune disease that is attributed to overstimulation of the thyroid glands by agonistic anti-thyrotropin receptor antibody, leading to hyperthyroidism and thyroid enlargement [1,2]
We analyzed the percentages of circulating CD4+ T cells in 27 patients with new onset GD and 27 gender- and age-matched healthy controls (HC), and we found that the percentages of CD4+ T cells in the GD patients were significantly higher than that in the HC (p,0.0001, Fig. 1)
We further analyzed the total numbers of Th22, Th17 and Th1 cells, and we found the total numbers of Th22 and Th17 cells in the GD patients were significantly higher than that in the HC (Fig. 1, P = 0.0020 and P = 0.0023, respectively)
Summary
Graves’ disease (GD) is an organ-specific autoimmune disease that is attributed to overstimulation of the thyroid glands by agonistic anti-thyrotropin receptor antibody (thyroid-stimulating antibody; TSAb), leading to hyperthyroidism and thyroid enlargement [1,2]. GD represents both the most common cause of, hyperthyroidism and an archetypical example of antibody-mediated organspecific autoimmunity. Since TSAb is a hallmark of GD T helper type 2 (Th2) responses have been associated with the pathogenesis of GD. Recent studies have suggested that other types of functional T cells, such as Th17 cells, play an important role in the pathogenesis of GD [4,5,6,7].
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
