Evaluation of IL-6 and IL-23 as Inflammatory Biomarkers in Patients with Thyroid Disorders
Downloads
The study included 90 participants divided into three groups: 40 patients with hypothyroidism, 26 patients with hyperthyroidism, and 24 healthy controls. Serum IL-6 and IL-23 concentrations were measured, A significant difference in serum IL-6 levels was observed among the three groups (F = 8.709, P < 0.001). The highest mean IL-6 concentration was recorded in the hyperthyroid group (46.7693 +/- 43.0165), followed by the control group (33.9306 +/- 31.2150), whereas the hypothyroid group showed the lowest concentration (16.6500 +/- 11.6646). Tukey's test demonstrated a significant difference between the hypothyroid and hyperthyroid groups, while the control group was not significantly different from either group. Serum IL-23 levels also differed significantly among the groups (F = 4.803, P = 0.011). The hyperthyroid group had the highest mean IL-23 concentration (26.9527 +/- 23.2794), followed by the control group (21.4263 +/- 11.3879), and the hypothyroid group had the lowest concentration (15.3270 +/- 8.9544).
[1] Q. Li, B. Wang, K. Mu, and J. A. Zhang, “The pathogenesis of thyroid autoimmune diseases: New T lymphocytes–cytokines circuits beyond the Th1–Th2 paradigm,” Journal of Cellular Physiology, vol. 234, no. 3, pp. 2204–2216, 2019.
[2] R. Wang et al., “Changes of serum cytokines in hyperthyroid Graves' disease patients at diagnosis and during methimazole treatment,” European Journal of Endocrinology, vol. 163, pp. 311–317, 2010.
[3] F. De Luca et al., “Serum interleukin-23 (IL-23) is increased in Hashimoto's thyroiditis,” Endocrine, vol. 46, pp. 390–394, 2014.
[4] T. Zake, S. Skuja, I. Kalere, V. Konrade, and V. Groma, “Upregulated tissue expression of T helper (Th) 17 pathogenic interleukin (IL)-23 and IL-1β in Hashimoto's thyroiditis but not in Graves' disease,” Endocrine Journal, vol. 66, no. 5, pp. 423–430, 2019.
[5] O. Saito et al., “Serum cytokine levels in Graves' disease,” Clinical Endocrinology, vol. 55, pp. 753–760, 2001.
[6] Q. Li, B. Wang, K. Mu, and J. A. Zhang, “Increased interleukin-23 in Hashimoto's thyroiditis disease induces autophagy suppression and reactive oxygen species accumulation,” Frontiers in Immunology, vol. 9, Art. no. 126, 2018.
[7] Y. Zhang et al., “Helper T cell 17 and regulatory T cell levels in peripheral blood of newly diagnosed patients with autoimmune thyroid disease: A meta-analysis,” Hormone and Metabolic Research, 2022.
[8] F. M. Botelho et al., “Increased circulating pro-inflammatory cytokines and Th17 lymphocytes in Hashimoto's thyroiditis,” European Journal of Endocrinology, vol. 160, pp. 789–798, 2009.
[9] C. Schinocca, C. Rizzo, S. Fasano, G. Grasso, L. La Barbera, F. Ciccia, and G. Guggino, “Role of the IL-23/IL-17 pathway in rheumatic diseases: An overview,” Frontiers in Immunology, vol. 11, Art. no. 637829, 2021.
[10] L. Zhou et al., “IL-6 programs TH-17 cell differentiation by promoting sequential engagement of the IL-21 and IL-23 pathways,” Nature Immunology, vol. 8, pp. 967–974, 2007.
[11] Y. Iwakura and H. Ishigame, “The IL-23/IL-17 axis in inflammation,” Journal of Clinical Investigation, vol. 116, no. 5, pp. 1218–1222, 2006.
[12] S. L. Gaffen, R. Jain, A. V. Garg, and D. J. Cua, “The IL-23–IL-17 immune axis: From mechanisms to therapeutic testing,” Nature Reviews Immunology, vol. 14, pp. 585–600, 2014.
[13] F. Annunziato et al., “From interleukin-23 to T-helper 17 cells: Human T-helper cell differentiation revisited,” Immunological Reviews, vol. 229, no. 1, pp. 138–146, 2009.
[14] Y. Wang, S. Fang, and H. Zhou, “Pathogenic role of Th17 cells in autoimmune thyroid disease and their underlying mechanisms,” Best Practice & Research Clinical Endocrinology & Metabolism, vol. 37, no. 2, Art. no. 101743, 2023.
[15] S. Janyga, D. Kajdaniuk, Z. Czuba, M. Ogrodowczyk-Bobik, A. Urbanek, B. Kos-Kudła, and B. Marek, “Interleukin (IL)-23, IL-31, and IL-33 play a role in the course of autoimmune endocrine diseases,” Endocrine, Metabolic & Immune Disorders–Drug Targets, vol. 24, no. 5, pp. 585–595, 2024.

