Abstract
Graves' disease (GD) is an autoimmune disease causing the overproduction of the thyroid hormone from thyroid gland. This disease is mainly the result of the production of antibodies against TSH receptors. Cytokines play an important role in orchestrating the pathophysiology in autoimmune thyroid disease. The regulatory role of IL-12 on TH1 cells has been proven. IL-27 and IL-35, members of IL-12 cytokine family, are two cytokines that have been newly discovered. IL-35 has been identified as a novel immunosuppressive and anti-inflammatory cytokine while IL-27 has both inflammatory and anti-inflammatory functions. The objective of the current study was to examine the changes in the serum level of the foregoing cytokines in GD patients in comparison to healthy controls. In this study, serum levels of IL-27 and IL-35 were determined by an ELISA method; anti TPO and anti Tg were measured by an RIA method in 40 new cases of Graves's disease. The findings were compared with 40 healthy controls. The results showed a significant difference between IL-27 and IL-35 regarding their serum levels with P values of 0.0001 and 0.024, respectively; anti TPO and anti Tg levels of the cases were also significantly different from controls (p < 0.001). The reduction in the serum levels of IL-27 and IL-35 in GD patients compared to normal subjects suggests the possible anti-inflammatory role of these cytokines in GD.
Highlights
Grave’s disease (GD) is an autoimmune thyroid disease characterized by thyrotoxicosis, diffuse goiter and the presence of autoantibody against thyroidstimulating hormone (TSH) receptor [1]
Many studies have shown that pro-inflammatory cytokines such as interleukin (IL)-2, IL-8, IL-6, tumor necrosis factor (TNF)-α and IL-17 are increased in the serum of GD patients [4]
Higher levels of anti-TPO and anti-Tg antibodies were observed in patients compared to the controls (p < 0.001, Figure 1)
Summary
Grave’s disease (GD) is an autoimmune thyroid disease characterized by thyrotoxicosis, diffuse goiter and the presence of autoantibody against thyroidstimulating hormone (TSH) receptor [1]. GD is a multifactorial disease whose etiology has not been fully fathomed, evidence shows that the imbalance between pro- and anti-inflammatory cytokines and production of aberrant autoantibodies play a pivotal role in the disease pathogenesis [1]. Many studies have shown that pro-inflammatory cytokines such as interleukin (IL)-2, IL-8, IL-6, tumor necrosis factor (TNF)-α and IL-17 are increased in the serum of GD patients [4]. The evaluation of the T helper (TH) subsets involvement in GD showed a TH2 bias immunological imbalance and an increase in TH1- and TH17-related cytokines compared to healthy controls [5,6,7]
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