Wang Xue-Rong, Xiao Jian-Ping, Wang De-Guang
Department of Nephrology, The Second Hospital of Anhui Medical University, Hefei, Anhui 230601, P.R. China.
Biomed Rep. 2021 Sep;15(3):76. doi: 10.3892/br.2021.1452. Epub 2021 Jul 23.
The present study aimed to investigate the levels of IL-36α and its association with disease activity in patients with systemic lupus erythematosus (SLE). A total of 60 patients with SLE and 29 healthy controls were enrolled in the present study. Disease activity was evaluated using the SLE disease activity index (SLEDAI). The serum levels of IL-36α, IL-36 receptor antagonist (IL-36Ra) and IL-17 were assessed using ELISA. The levels of IL-36α in patients with SLE were significantly higher compared with those of healthy controls. There was a significant increase in IL-36α in the active SLE group (SLEDAI score ≥5) compared with that of the healthy controls (P<0.001). The serum IL-36α levels were higher in patients with active SLE than in patients with quiescent disease (P=0.012). IL-36Ra was downregulated in patients with SLE (P=0.007). The serum IL-17 levels were elevated in patients with SLE (P=0.036), and a positive correlation was observed between the IL-36α and IL-17 levels (r=0.453, P=0.003). The serum IL-36α levels were associated with SLEDAI (r=0.374, P=0.003), proteinuria (r=0.329, P=0.010) and complement 3 (r=-0.336, P=0.009). Patients who were receiving glucocorticoid treatment had lower IL-36α levels than those who were not receiving glucocorticoid treatment (P=0.003). Patients with lupus nephritis had higher serum IL-36α levels compared with those found in patients without lupus nephritis (P=0.037). The serum IL-36α concentration was elevated in patients with SLE, and was correlated with disease activity and IL-17 levels. The aberrant serum IL-36α levels observed in the present study and its clinical association with SLE suggest the important role of IL-36α in onset and progression of SLE. In addition, the association of IL-36α with IL-17 level indicates its involvement in the regulation of T helper 17 cytokines.
本研究旨在调查系统性红斑狼疮（SLE）患者中白细胞介素-36α（IL-36α）的水平及其与疾病活动度的关系。本研究共纳入了60例SLE患者和29例健康对照者。采用SLE疾病活动指数（SLEDAI）评估疾病活动度。使用酶联免疫吸附测定（ELISA）法检测血清中IL-36α、白细胞介素-36受体拮抗剂（IL-36Ra）和白细胞介素-17（IL-17）的水平。与健康对照者相比，SLE患者的IL-36α水平显著更高。与健康对照者相比，活动期SLE组（SLEDAI评分≥5）的IL-36α显著升高（P<0.001）。活动期SLE患者的血清IL-36α水平高于病情静止期患者（P=0.012）。SLE患者的IL-36Ra表达下调（P=0.007）。SLE患者的血清IL-17水平升高（P=0.036），且IL-36α水平与IL-17水平呈正相关（r=0.453，P=0.003）。血清IL-36α水平与SLEDAI（r=0.374，P=0.003）、蛋白尿（r=0.329，P=0.010）和补体3（r=-0.336，P=0.009）相关。接受糖皮质激素治疗的患者IL-36α水平低于未接受糖皮质激素治疗的患者（P=0.003）。与无狼疮性肾炎的患者相比，狼疮性肾炎患者的血清IL-36α水平更高（P=0.037）。SLE患者的血清IL-36α浓度升高，且与疾病活动度和IL-17水平相关。本研究中观察到的血清IL-36α水平异常及其与SLE的临床关联表明IL-36α在SLE的发病和进展中起重要作用。此外，IL-36α与IL-17水平的关联表明其参与辅助性T细胞17细胞因子的调节。
