Role of interlekin-35 as a biomarker in patients with newly diagnosed Hashimoto’s thyroiditis

Year, pages: 2016, 55 - 61

Interleukin-35 (IL-35), an interleukin-12 (IL-12) cytokine family member, is shown to be a potent immunosuppressive and anti-inflammatory cytokine. Inducible regulatory T cells (Tregs) produce IL-35 that mediates the immune inhibitory function of Tregs. Growing evidence revealed that upregulation of IL-35 expression may play a critical role in the prevention of autoimmune diseases in various experimental autoimmunity models and vice versa. Hashimoto’s thyroiditis (HT) is considered to be a Treg cell-related autoimmune disease with loss of self-tolerance. One hundred-twenty eight subjects, newly diagnosed hypothyroid HT patients [56 overt (Group 1), 72 subclinical hypothyroid (Group 2)] and 38 healthy controls (Group 3) were enrolled in the study. The levels of serum IL-35 were determined by enzyme-linked immunosorbent assay (ELISA). Serum IL-35 levels were lower in the HT group when compared with subclinical HT group [304.5 (834.6) pg/ml vs. 636.1 (1542.0) pg/ml, p=0.004] and control cases [304.5 (834.6) pg/ml vs. 1064.7 (2526.8) pg/ml, p<0.001]. Serum IL-35 levels were inversely associated with thyroid stimulating hormone (TSH; rs=–0.396, p<0.001) and anti-thyroid peroxidase antibodies (TPOAb; rs=–0.571, p<0.001) in whole group. Serum IL-35 were negatively associated with TSH (rs=–0.264, p=0.003) and TPOAb (rs=–0.735, p<0.001) in patients with Hashimoto’s thyroiditis (Group 1 + Group 2). The results suggest that IL-35 may play a role in the pathogenesis of HT.

Yilmaz, H., Cakmak, M., Ceydilek, B., Aktas, A. 2016. Role of interlekin-35 as a biomarker in patients with newly diagnosed Hashimoto’s thyroiditis. In ENDOCRINE REGULATIONS, vol. 50, no.2, pp. 55-61. 1210-0668. DOI: https://doi.org/10.1515/enr-2016-0009

Yilmaz, H., Cakmak, M., Ceydilek, B., Aktas, A. (2016). Role of interlekin-35 as a biomarker in patients with newly diagnosed Hashimoto’s thyroiditis. ENDOCRINE REGULATIONS, 50(2), 55-61. 1210-0668. DOI: https://doi.org/10.1515/enr-2016-0009

Publisher: de Gruyter Open