Endocrine Abstracts

Introduction: Th17 cells and their hallmark cytokine IL-17A were reported to be involved in the development of autoimmune orchitis and encephalomyelitis by impairing the integrity of the blood–testis and blood–brain barrier integrity and by inducing local inflammation. However, the role of IL17A in autoimmune thyroid disease is still debatable.

The aim of our study was to estimate immunoexpression of IL-17A in the thyroid tissue of patients with Hashimoto’s thyroiditis (HT) and Graves’ disease (GD) compared to control group.

Materials and methods: 35 adult patients presenting 18 cases of HT, seven of GD, and ten cases of ordinary colloidal goiter without autoimmune component undergoing thyroidectomy were enrolled in this study. Immunostaining was performed using an anti-IL17A antibody; macrophages were visualized by CD68 immunohistochemistry. Results were expressed in a semiquantitative manner.

Results: The highest expression level of IL17A in the follicular epithelial cells was observed in HT patients, furthermore, in HT and GD patients it was significantly higher than that in control group (P<0.001; P=0.007, respectively). CD68-positive macrophages of both intra- and extrafollicular localization were observed in all tissue samples. The largest number of CD68-positive cells within follicular lumen was found in HT patients (P=0.001). CD68 positivity observed in GD patients was higher compared to nodular goiter, but the difference was not significant (P=0.064). A strong positive correlation was found between the degree of inflammatory cell infiltration and the number of CD68-positive macrophages in HT patients (r=0.912, P=0.0001). In addition, HT patients demonstrated a moderate positive correlation between CD68 and IL17A immunopositivity (r=0.631, P=0.005).

Conclusion: Overexpression of IL17A in the follicular epithelial cells associated with the presence of intrafollicular macrophages and high inflammatory infiltration degree in HT patients may indicate the involvement of IL17 in thyroid follicular barrier impairment.