Abstract :
Hashimoto's Thyroiditis (HT) are identified by chronic thyroid gland inflammation with uncertain etiologies, is it an autoimmune illness. Interleukin-33 and IL-35 have recently been discovered to play a role in progression of numerous autoimmune disorders. Interleukin-35 (IL-35), a cytokine family member of interleukin-12, has been demonstrated to be an effective immunosuppressive as well as anti-inflammatory action. Treg generate IL-35, which is responsible for Tregs' immunological suppressive role. Increasing IL-35 level through experimental models may play an important function in avoiding Auto - immune illnesses. Furthermore, HT is hypothesized to be a regulatory T cell associated auto-immune disease marked by a lack of self-tolerance. Interleukin-33 (IL-33) has recently been discovered to play a role in progression of numerous autoimmune disorders. In this study, the role of IL-33 and IL-35 in development and pathogenesis of HT are studied. One hundred-twenty subjects enrolled in this study, The levels of IL-33, IL-35 in serum are measured. And the samples divided as 40 newly diagnosed HT patients before treatment classified into (Euthyroid HT, Subclinical HT and Overt HT) based on thyroid function test presentation, 40 non immune hypothyroidism and 40 healthy controls were determined by enzyme-linked immunosorbent assay (ELISA). and Electrochemiluminescence immunoassay (ECLIA) method. The serum IL-33 were significantly elevated in newly diagnosed HT patients, compared to non immunehypothyroidism and healthy control with an significantly decreased in IL -35 in newly diagnosed HT when compare with non- immunehypothyroidism and healthy control.
