Ankylosing spondylitis (AS) is a common chronic progressive inflammatory autoimmune disease. T helper 17 (Th17) cells are the major effector cells mediating AS inflammation. Histone 3 Lys 27 trimethylation (H3K27me3) is an inhibitory histone modification that silences gene transcription and plays an important role in Th17 differentiation. The objective of this study was to investigate the expression of H3K27me3 in patients with AS and to explore its epigenetic regulation mechanism of Th17 differentiation during AS inflammation. We collected serum samples from 45 patients with AS at various stages and 10 healthy controls to measure their Interleukin-17 (IL-17) levels using ELISA. A quantitative polymerase chain reaction was used to quantify the mRNA levels of RORc and the signaling molecules of the JAK2/STAT3 pathway, JMJD3, and EZH2. Additionally, Western blot analysis was performed to quantify the protein levels of H3K27me3, RORγt, JAK2, STAT3, JMJD3, and EZH2 in cell protein extracts. The results showed that H3K27me3 expression in peripheral blood mononuclear cells (PBMCs) was significantly lower in patients with active AS compared to both the normal control groups and those with stable AS. Moreover, a significant negative correlation was observed between H3K27me3 expression and the characteristic transcription factor of Th17 differentiation, RORγt. We also discovered that patients with active AS exhibited significantly higher levels of JMJD3, an inhibitor of H3K27 demethylase, compared to the normal control group and patients with stable AS, while the expression of H3K27 methyltransferase (EZH2) was significantly lower. These findings suggest that H3K27me3 may be a dynamic and important epigenetic modification in AS inflammation, and JMJD3/EZH2 regulates the methylation level of H3K27me3, which may be one of the key regulatory factors in the pathogenesis of AS. These findings contribute to our understanding of the role of epigenetics in AS and may have implications for the development of novel therapeutic strategies for AS.

强直性脊柱炎（AS）是一种常见的慢性进行性炎症性自身免疫性疾病。辅助 T 17 (Th17) 细胞是介导 AS 炎症的主要效应细胞。组蛋白 3 Lys 27 三甲基化 (H3K27me3) 是一种抑制性组蛋白修饰，可沉默基因转录并在 Th17 分化中发挥重要作用。本研究旨在探讨H3K27me3在AS患者中的表达情况，探讨其在AS炎症过程中Th17分化的表观遗传调控机制。我们收集了 45 名不同阶段的 AS 患者和 10 名健康对照者的血清样本，使用 ELISA 测量他们的白细胞介素 17 (IL-17) 水平。使用定量聚合酶链反应来定量 RORc 和 JAK2/STAT3 途径、JMJD3 和 EZH2 信号分子的 mRNA 水平。此外，还进行蛋白质印迹分析以量化细胞蛋白提取物中 H3K27me3、RORγt、JAK2、STAT3、JMJD3 和 EZH2 的蛋白水平。结果显示，与正常对照组和稳定期AS患者相比，活动期AS患者外周血单个核细胞（PBMC）中H3K27me3的表达显着降低。此外，H3K27me3 表达与 Th17 分化的特征转录因子 RORγt 之间存在显着负相关。我们还发现，与正常对照组和稳定AS患者相比，活动性AS患者的JMJD3（一种H3K27去甲基酶抑制剂）水平显着升高，而H3K27甲基转移酶（EZH2）的表达显着降低。这些发现提示H3K27me3可能是AS炎症中动态且重要的表观遗传修饰，JMJD3/EZH2调节H3K27me3的甲基化水平，这可能是AS发病机制中的关键调控因素之一。这些发现有助于我们了解表观遗传学在 AS 中的作用，并可能对 AS 新型治疗策略的开发产生影响。