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This is a Animal Study study (also classified as: Experimental Study).

September 23, 2025Open Access

P11 - Preclinical evaluation of calcitriol’s immunomodulatory role in Graves’ disease

Key Points

Calcitriol treatment in vitamin D-deficient GD mice reduced tshr abs and maintained t4 levels similar to controls.
At week 6, elevated tshr abs were observed in both GD and GD+calcitriol groups, indicating immune dysregulation.
The preclinical model involved GD mice receiving calcitriol thrice weekly and monitoring serum levels via ELISA.
These findings suggest calcitriol may offer a novel therapeutic avenue in managing graves disease and warrant further research.

Abstract

Abstract Introduction Graves’ disease (GD) is an autoimmune thyroid disorder characterized by immune dysregulation. Vitamin D exhibits immunomodulatory effects and may influence disease activity. Although some studies suggest an association between vitamin D status and GD, evidence remains limited. Active vitamin D (calcitriol) may exert more potent immunoregulatory effects. Purpose This study explores its therapeutic potential in a preclinical GD model. Methods To evaluate the therapeutic effect of calcitriol in vitamin D-deficient GD mice, Rosa26ₕTSHRa (Balb/C) mice were fed a vitamin D-deficient diet for four weeks prior to the experiment. Mice were divided into three groups: Control (n=6), GD (n=6), and GD+calcitriol (n=6). GD and GD+calcitriol groups received 250 U of TAT-Cre by intramuscular injection into one thigh at 8 weeks, followed by injection into the opposite thigh 3 weeks later. The GD+calcitriol group was treated with calcitriol (5 µg/kg, subcutaneously, three times per week) from week 7. Serum T4 and TSHR Abs were measured by ELISA using blood samples collected at weeks 6 and 13. Results At week 6, TSHR Abs in both the GD and GD+calcitriol groups were significantly elevated compared to the control group, with similar levels between the two groups, and T4 levels began to rise. At week 13, although this difference did not reach statistical significance, the GD+calcitriol group showed a greater reduction in TSHR Abs compared to the GD group. The GD group had significantly higher T4 levels than the control group, whereas the GD+calcitriol group maintained T4 levels similar to the control group. Conclusion Calcitriol treatment in a vitamin D-deficient GD mouse model demonstrated potential to modulate autoimmune activity by reducing TSHR Abs and preventing excessive increases in serum T4. These results suggest that active vitamin D may have a therapeutic role in managing GD, warranting further investigation in preclinical and clinical settings.

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