Furthermore, neutralization of leptin decreases the frequency of Th17 cells in vitro. Current study has revealed an increased leptin involvment in Hashimoto’s thyroiditis associated with an increased number of Th17 cells. Hashimoto’s thyroiditis (HT), also known as chronic lymphocytic thyroiditis, is an organ-specific autoimmune disease characterized by the presence of goitre, lymphocytic infiltration and serum thyroid autoantibodies. HT is a complex disease caused by overt autoimmune response, multiple gene susceptibility and environmental factors. Previous reports have shown that autoreactive CD4+ T cells

against thyroid antigens, especially interleukin EX527 (IL)-12-dependent T helper type 1 (Th1) cells, are involved in the disease progression of HT [1]. Furthermore, several reports, including our recent studies, have described that increased CD4+ Th17 cells might

be involved in the pathogenesis of HT [2, 3]. However, the mechanisms leading to increased Th17 cells in HT patients remain poorly understood. Leptin is a 16 kDa non-glycosylated polypeptide encoded by the obese (ob) gene, consisting of four interconnected anti-parallel α-helices, which is in high similarity to members of the long-chain helical cytokines, such as IL-6, IL-11, IL-12 and granulocyte–colony-stimulating factor (G-CSF) [4-6]. As an adipocyte-derived hormone, leptin regulates this website energy homeostasis [7], neuroendocrine function [8], reproduction [9], angiogenesis [10] and haematopoiesis [11]. Many studies have characterized a critical role of leptin in T cell activation and function. We have shown recently that leptin plays an indispensable role in the maturation and function of dendritic cells and natural killer cells [12, 13]. Accumulating evidence suggests that leptin acts as a proinflammatory cytokine in immune responses, which is involved in the pathogenesis of various autoimmune diseases [6]. Importantly,

it has been reported that leptin is implicated in the pathogenesis of multiple sclerosis (MS) patients and experimental autoimmune encephalomyelitis (EAE) mice by altering the balance of Th1/Th2 and suppression of CD4+CD25+ regulatory T cell (Treg) proliferation [2, 14, 15]. However, little is known regarding the role of leptin ID-8 in the disease pathogenesis of HT. In this report, we investigate the change of plasma leptin and CD4+ T cell-derived leptin in HT patients, as well as the relationship between leptin and Th17 cells. We found that leptin neutralization affected the formation of Th17 cells in vitro. Our findings will provide further understanding regarding the role of leptin in the disease pathogenesis of HT. A total of 27 patients with Hashimoto’s thyroiditis (HT) were enrolled into the study. The main clinical data of these patients are shown in Table 1.