Promotion of IL‑17/NF‑κB signaling in autoimmune thyroid diseases

Abstract

IL-17 and other cytokines have a number of immunomodulatory effects on thyroid cells. The present study investigated the changes and correlations amongst IL-17, NF-κB, IL-6, IL-10, interferon-γ (IFN-γ), TNF-α, IL-2 and IL-4 in patients with different autoimmune thyroid diseases in order to further clarify the pathogenesis of autoimmune thyroid disease. A total of 82 patients with autoimmune thyroid diseases (41 with Graves' disease and 41 with Hashimoto's thyroiditis) and 53 healthy controls were enrolled. All relevant thyroid hormones were detected by electrochemiluminescence analyzer. The serum levels of IL-17 and other cytokines were detected using flow cytometry, NF-κB was detected by ELISA, reverse transcription-quantitative PCR was used to detect the protein expression of various mRNAs, and the correlations between IL-17 and these factors were analyzed. Significant differences occurred amongst all groups. NF-κB, TNF-α, IL-6, IL-17 and their mRNA levels were significantly higher in the healthy controls compared with those in the patients; whereas IFN-γ and IL-10 levels were significantly lower in the healthy controls compared with those in the patients . Correlation analysis showed that the expression levels of IL-17 and its mRNA were significantly positively correlated with the expression levels of NF-κB, IL-6, thyroid peroxidase antibody, thyroid gland globulin, thyroglobulin antibody, TNF-α and IFN-γ, and were also significantly negatively correlated with IL-10 . These findings suggested that IL-17 was elevated in patients with autoimmune thyroid disease and that IL-17 could activate the NF-κB signaling pathway, stimulate the production and release of inflammatory factors such as TNF-α, IL-6 and IFN-γ and participate in the pathogenesis of autoimmune thyroid injury.

Alteration in gut microbiota is associated with immune imbalance in Graves’ disease

“…Pivotal inflammatory mediators, including IL-17, TNF-α, and IL-6, are integral to GD pathophysiology. IL-17, a notable proinflammatory cytokine, instigates the NF-κB signaling cascade, resulting in the subsequent release of TNF-α and IL-6 ( Lu et al., 2023 ). Concurrently, heightened activity of the TNF-α/TNFR or IL-6/STAT3 pathways also promotes Th17 differentiation and IL-17 production ( Pesce et al., 2022 ).…”

Exome sequencing to explore the possibility of predicting genetic susceptibility to the joint occurrence of polycystic ovary syndrome and Hashimoto’s thyroiditis

“…Chronic inflammation is a hallmark of both HT and PCOS ( 73 , 74 ). In patients with HT, the expression of interleukin (IL)-17 was elevated and was significantly correlated with the levels of thyroid hormone, anti-TPO, and anti-Tg antibodies ( 75 ). In turn, IFN-γ and IL-10 levels were significantly lower in the HT patients compared with the controls.…”

Role of oxidative stress and IL-17 induced inflammatory cytokines in thyroid carcinoma with Hashimoto's thyroiditis

“…Interleukin-17 is a powerful cytokine that can cause cascade growth of in ammation, and can also increase the level of local in ammatory response by stimulating various cytokines such as IL-1β and IL-6 [18].Our previous studies have shown [19] that IL-17 can activate the NF-κB signaling pathway, stimulate the production and release of in ammatory factors such as TNF-α, IL-6 and IFN-γ, and participate in autoimmune thyroid injury.Studies have proved that in ammation is also closely related to the onset of tumors, and in ammatory cells can promote the occurrence and development of cancer [20].The results showed that compared with the control group, IL-17A, IL-1β and IL-6 in PTC+HT, PTC+HT and HT groups were signi cantly increased, and further increased in PTC+HT group. Activated in ammatory factors destroyed thyroid follicular cells and tissues, resulting in thyroid hormone level disturbance and increased antibody production.…”