SERUM INTELEUKIN-22 (IL-22) IS INCREASED IN HASHIMOTO'S THYROIDITIS (HT) COMAPRED WITH NON AUTOIMMUNE THYROID DISEASES AND HEALTHY CONTROLS.

Objectives. HT is an archetype for organ-specific autoimmune diseases (AID), that is considered to be Th1-related. Recent studies revealed that Th17 lymphocytes (producing mostly IL-17, IL-21 and IL-22) play a major role in numerous AID commonly thought to be Th1 diseases. Few data are available in the literature on the role for Th17 cells in HT. Methods. Using IL-22 Quantikine ELISA Kit (lower limit of detection 0.7 pg/ml) we assayed serum levels of IL-22 in three groups of persons: HT patients (group A, n= 40, 5 males and 35 females, age 42±16 years), non-HT patients with nodular euthyroid goiter (group B, n= 22, 2 males and 20 females, age 47±11 years) and an age- and sex-matched group of disease-free, healthy persons (group C). HT patients were euthyroid when sampled. Data are expressed as mean ± SD (pg/ml). Statistical analysis is by the two-tailed Student’s t test. Results. IL-22 levels were 43±37.4 pg/ml in HT patients, 18.7±17 pg/ml in group B and 20.7±12.7 pg/ml in group C. Because IL-22 levels in groups B and C were similar, they were pooled (19±15 pg/ml). These levels were significantly lower (p<0.001) than in the HT group. In HT patients no significant correlation was found between serum levels of IL-22 and Tg-Ab and/or TPO-Ab levels. Furthermore, IL-22 values did not differ in HT patients positive for both Tg-Ab and/or TPO-Ab compared with HT patients with positivity for only one of these two autoantibodies. Conclusions. Serum IL-22 is increased in HT, as compared to autoimmune diseases-free individuals. Our data do not support a strong role of Th17 cells, as assessed by their main soluble mediator IL-22, in the pathogenesis of HT.