Abstract

Recent incidence rates for Hashimoto's thyroiditis (HT) and hypothyroidism are higher than those of previous studies. Previous studies indicated that T helper cells may have a major role in the pathogenesis and development of HT, but there is no consensus in the literature. The aim of the present study was to explore the peripheral T helper cell response in the different stages of HT. In this cross-sectional study, we performed flow cytometry analysis to determine the various T cell subsets of 389 patients with HT (34 patients with HT who developed overt hypothyroidism, and 148 patients with HT who developed subclinical hypothyroidism), as well as 51 healthy controls. Anti-thyroid antibodies, and thyroid function were measured. The findings demonstrated that the proportion of peripheral Th1 cells was significantly lower in patients with HT than in healthy euthyroid controls (P<0.001), and the proportion of peripheral Th2, Treg cells was significantly higher in patients with HT than in healthy euthyroid controls (P<0.001). Therefore the Th1/Th2 ratio was significantly lower in HT patients than in healthy euthyroid controls (P<0.001). The Th17/Treg ratio in HT patients was significantly lower than that control subjects (P<0.001). Th1 proportions in patients with overt hypothyroidism HT were significantly higher than in subclinical hypothyroidism HT patients (P=0.031). In conclusion, the findings of the present study demonstrated that there is an increased immune deviation of Th1 lymphocytes and compensatory accelerating activity of Treg cells in HT, and the peripheral Th1 cells from the HT patients correlated to the developmental stage of hypothyroidism.

Full Text
Paper version not known

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 call

Disclaimer: 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.