Interleukin (IL)-23, IL-31, and IL-33 Play a Role in the Course of Autoimmune Endocrine Diseases

免疫学 内分泌系统 医学 白细胞介素15 白细胞介素 细胞因子 内科学 激素
作者
Szymon Janyga,Dariusz Kajdaniuk,Zenon Czuba,Monika Ogrodowczyk-Bobik,Agata Urbanek,Beata Kos‐Kudła,Bogdan Marek
出处
期刊:Endocrine, metabolic & immune disorders [Bentham Science Publishers]
卷期号:24 (5): 585-595 被引量:3
标识
DOI:10.2174/1871530323666230908143521
摘要

Background: Interleukins (IL)-23, 31, and 33 are involved in the regulation of T helper 17 (Th17)/regulatory T (Treg) cells balance. The role of IL-23, 31 and 33 in non-endocrine auto-immune diseases has been confirmed. Data on the involvement of these cytokines in endocrine autoimmune diseases are limited. Objective: This study aimed to determine the involvement of cytokines regulating the T helper 17 (Th17)/regulatory T (Treg) cells axis in the course of autoimmune endocrine diseases. Methods: A total number of 80 participants were divided into 4 groups: the autoimmune polyen-docrine syndrome (APS) group consisting of APS type 2 (APS-2) and type 3 (APS-3) subgroups, the Hashimoto's thyroiditis (HT) group, the Graves’ disease (GD) group and the control (C) group. Fifteen cytokines related to Th17 and Treg lymphocytes were determined in the serum of all participants. Results: Higher levels of IL-23 and IL-31 were found in the APS, GD, and HT groups compared to the C group. Higher levels of IL-23 and IL-31 were also observed in the APS-2 group, in contrast to the APS-3 group. Correlation analysis of variables in the groups showed a statistically signifi-cant correlation between the cytokines IL-23, IL-31, and IL-33 in the APS and APS-2 groups, but no correlation in the APS-3 and C groups. Conclusion: IL-23 and IL-31 are independent factors in the course of HT, GD, and APS-2, in contrast to APS-3. The positive correlation between IL-23 and IL-31, IL-23 and IL-33, and be-tween IL-31 and IL-33 in the APS, APS-2 groups, but the lack of correlation in the APS-3 and C groups may further suggest the involvement of these cytokines in the course of Addison's disease.
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