Endocrine Abstracts

Introduction: Recently, Th17 cells and their cytokines were identified to play an important role in the pathogenesis of thyroid autoimmunity. IL-23, produced by antigen presenting cells, is required for survival and differentiation of Th17 cells, and is known to guide T cells toward the Th17 phenotype. Its serum levels are increased in several autoimmune diseases, including Hashimoto’s thyroiditis (HT), however, the expression level of IL-23 within thyroid tissue assessed by immunohistochemistry has not been addressed thoroughly before. The aim of our study was to estimate the levels of immunoexpression and distribution of IL-23 within thyroid tissue of patients with HT and Graves’ disease (GD) and compare them with controls.

Materials and Methods: Forty seven adult patients presenting 21 cases of HT, 8 of GD, and 18 cases of ordinary colloidal goiter without autoimmune component, which served as control group, were enrolled in this study. Immunostaining was performed using an anti-IL-23 antibody (Santa Cruz Biotechnology, CA, dilution 1:50). Levels of immunopositivity for IL-23 were defined semiquantitatively.

Results: In HT patients the expression of IL-23 was detected both in the abundant inflammatory lymphocytic infiltrates characteristic of HT and follicular epithelial cells, whereas tissues obtained from GD patients demonstrated the weak thyrocytic expression predominantly. Majority of patients in controls showed negative or occasional expression of IL-23. The highest IL-23 immunopositivity was observed in HT patients, furthermore, it was significantly higher compared to the control group and GD (P<0.001; P=0.043, respectively). No difference was found between the expression of IL-23 in GD patients and the control group (P=0.324). Additionally, weak expression of IL-23 was observed in connective tissue septae and blood vessels in most HT patients.

Conclusion: Overexpression of IL-23 might play a role in the pathogenesis of HT, guiding T cells towards the Th17 phenotype and promoting the autoimmune inflammation of the thyroid gland.