ESPE Abstracts

Background: Graves’ disease (GD) involves autoimmunity against TSH receptor (TSHR) bearing cells, leading to hyperthyroidism and often orbitopathy. When hyperthyroidism is treated with radioactive iodine (RAI), exacerbation of the orbital disease can occur.

Objective and hypotheses: We hypothesized that RAI has immune effects affecting the balance between auto-reactive T cells and T cells with regulatory properties.

Method: We monitored lymphocyte populations in peripheral blood of GD patients, patients with non-autoimmune goiter (NG), and healthy controls.

Results: Circulating T cell interferon gamma production in the presence of TSHR peptides was measured in ten GD patients and ten healthy controls. Significant response to at least one peptide was measured in 2/10 and 4/10 GD patients before and after RAI therapy, respectively, and in none of the controls. Regulatory CD4⁺CD25^highFOXP3⁺T cells (Tregs) and Vα24⁺Vβ11⁺CD3⁺ natural killer T cells (NKT) were counted by flow cytometry in 16 GD patients and in five NG patients before and 1 month post-RAI treatment, as well as in seven untreated healthy subjects over the same time period. Variance of Tregs and NKT cells before and after RAI therapy was greater in GD patients compared to NG (Treg: P=0.0053; NKT: P=0.0117) and to controls (Treg: P<0.0001; NKT: P=0.0217). Post-RAI therapy, frequency of Tregs was positively correlated with NKT cells numbers in GD patients (P=0.0422).

Conclusion: Collectively, RAI therapy has a mild effect on auto-reactive T cells specific to thyroid peptides. However, variation in Tregs and NKT cells after thyroid radiation appears to be greater in Graves’ disease patients.