Yilmaz, HakkiÇakmak, MuzafferCeydilek, BilgeDemir, CananAktas, Aynur2025-10-242025-10-2420161336-03291210-0668https://doi.rog/10.1515/enr-2016-0009https://hdl.handle.net/20.500.12899/3160Objective. 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. Methods. 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 immunosor-bent assay (ELISA). Results. 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). Conclusion. The results suggest that IL-35 may play a role in the pathogenesis of HT. © 2020 Elsevier B.V., All rights reserved.eninfo:eu-repo/semantics/openAccessAutoimmunityHashimoto’s thyroiditisHypothyroidismIL-35InflammationArticle10.1515/enr-2016-00095025561275606372-s2.0-84981287970Q3