Intrathyroid injection of dexamethasone inhibits Th2 cells in Graves' disease.

Ke He,Yun Hu,Xiao-Ming Mao,Xiao-Mei Liu,Bing-Li Liu,Peng Jiang

doi:10.20945/2359-3997000000244

Ke He, Yun Hu + Show 4 more

Open Access

https://doi.org/10.20945/2359-3997000000244

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Abstract

Intrathyroid injection of dexamethasone (IID) was used for decrease the relapse rate of hyperthyroidism in the treatment of Graves' disease (GD), but the mechanism is still unclear. We aimed to explore the effect of IID on T help (Th)1/Th2 cells and their chemokine in patients with GD. A total of 42 patients with GD who were euthyroidism by methimazole were randomly divided into IID group (n = 20) and control group (n = 22). Thyroid function and associated antibody, Th1/Th2 cells proportion, serum CXCL10 and CCL2 levels, and CXCR3/CCR2 mRNA expression in peripheral blood mononuclear cells before and after 3-month IID treatment were tested by chemiluminescence assay, Flow cytometry, ELISA, and real-time PCR, respectively. Thyroid follicular cells were stimulated by IFN-γ and TNF-α and treated with dexamethasone in vitro. CXCL10 and CCL2 levels in supernatant were determined. After 3-month therapy, the proportion of Th2 cells and serum CCL2 levels, as well as TPOAb, TRAb levels and thyroid volume decreased in IID group (p < 0.05). However, the proportion of Th1 and CXCL10 levels had no change in IID group and control (p > 0.05). The CXCR3/CCR2 ratio had no change in both groups (p > 0.05). IID therapy could inhibit peripheral Th2 cells via decreasing CCL2 level in peripheral blood, and this result partly explain the effects of IID therapy on prevention of relapse of GD. Arch Endocrinol Metab. 2020;64(3):243-50.

Highlights

Graves’ disease (GD) is a thyroid-specific autoimmune disease that thyroid-stimulating antibody (TSAb) stimulates thyroid-stimulating hormone receptor (TSHR) and leads to overproduction of thyroid hormones
The clinical characteristics of patients before and after the therapy are shown in Table 1, and there was no significant difference between control and injection of DEX (IID) groups at the beginning of the therapy
After 3-month therapy, TSH, FT4, thyroglobulin antibody (TGAb), thyroid peroxidase antibody (TPOAb), thyrotropin receptor antibody (TRAb) and thyroid volume had no change in control while the TPOAb, TRAb and thyroid volume decreased in IID group (p < 0.05)

Summary

INTRODUCTION

Graves’ disease (GD) is a thyroid-specific autoimmune disease that thyroid-stimulating antibody (TSAb) stimulates thyroid-stimulating hormone receptor (TSHR) and leads to overproduction of thyroid hormones. Several studies showed a significant increase in Chemokine (C-X-C motif) ligand 10 (CXCL10, named IP-10) strongly associated with Th1-mediated immune responses in thyroid tissue specimens and serum obtained from recent-onset GD patients [9,10]. Increased level of CCL2 has been observed both in peripheral blood of patients with autoimmune thyroid disease (AITD) [15] and supernatant of thyroid follicular cells from GD patients after stimulated by IFN-γ and TNF-α in vitro An intrathyroid injection of DEX (IID) could effectively reduce the relapse rate in GD patients after withdrawing MMI treatment [17]. Blood from all of the patients was collected before and after the 3-month therapy, Th1/Th2 cells were tested immediately, while serum was kept frozen at –80 °C until the thyroid hormones, anti-thyroid antibodies, CXCL10 and CCL2 were tested.

RESULTS

DISCUSSION

Month B