Immunoexpression of the CD30 ligand-CD30 and IL-6-IL-6R signals in thyroid autoimmune diseases

Abstract

To elucidate the role of Th2 cytokines in autoimmune thyroid diseases, we have studied by immunohistochemistry the expression of two Th2 ligand/receptor systems (CD30-L/CD30 and IL-6/IL-6R) in goitrous Graves’ disease (GD) and Hashimoto’s thyroiditis (HT). A total number of 50 nodular goiters (NG), including 10 GD showing a lymphoid aggregate grade I, 30 HT 8 of which had a lymphoid aggregate of grade I, 12 of grade II and 10 grade III, and 10 colloid goiters have been evaluated. In addition, 5 normal thyroids were included in the study as controls. Reactivity of ligand and cognate receptor of both CD30-L/CD30 and IL-6/IL-6R pathways was observed in a greater proportion of GD, compared to HT (P<0.005). In HT, the expression of CD30-L/CD30 system was detected more frequently than IL-6/IL-6R (P<0.05) and showed an inverse correlation with the grade of lymphoid aggregate, whereas IL-6/IL-6R correlated positively with lymphocyte infiltration (P<0.05). Based on our results concerning a dominance of Th2 cytokines in GD, we postulate that CD30-L/CD30 and IL-6/IL-6R systems could play a major role in the pathogenesis of GD. However, the expression of CD30L/CD30 and IL-6/IL-6R in HT suggests that Th2 mechanisms are involved also in tissue damage of HT. The two systems could contribute to drive the autoimmune response skewing toward a Th2 phenotype and this appears to be correlated with the lymphoid aggregate grade.