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目的探讨白细胞介素37(IL-37)对细菌脂多糖(LPS)诱导的小鼠树突状细胞(DC)活化的调节作用。方法应用GM-CSF和IL-4诱导小鼠骨髓细胞向DC分化,抗CD11c磁珠分选DC。IL-37预处理DC后,进行LPS刺激。流式细胞术检测DC表面共刺激分子(CD80、CD86)表达水平,实时荧光定量PCR检测肿瘤坏死因子α(TNF-α)、IL-6和IL-1αmRNA表达水平,流式细胞微球芯片试剂盒(CBA试剂盒)检测细胞培养上清中IL-1α、IL-6、TNF-α等因子的浓度。结果 DC诱导成功,磁珠分选能够获得高纯度的DC(>90%)。IL-37降低LPS诱导的DC表面共刺激分子CD80、CD86的表达,并抑制DC合成IL-1α、IL-6、TNF-α。结论 IL-37可以通过降低共刺激分子和炎症因子的表达抑制LPS刺激的DC活化。
Objective To investigate the regulatory effect of interleukin-37 (IL-37) on activation of dendritic cells (DCs) induced by bacterial lipopolysaccharide (LPS) in mice. Methods The bone marrow cells of mice were induced to differentiate into DC by GM-CSF and IL-4, and DCs were sorted by anti-CD11c magnetic beads. After pretreating DC with IL-37, LPS stimulation was performed. Flow cytometry was used to detect the expression of costimulatory molecules (CD80, CD86) on DC surface. The mRNA expression of TNF-α, IL-6 and IL-1α was detected by real-time fluorescence quantitative PCR. The concentration of IL-1α, IL-6, TNF-αand other factors in the cell culture supernatant was detected by the kit (CBA kit). Results DC induction success, magnetic beads sorting can obtain high purity DC (> 90%). IL-37 decreased the LPS-induced DC surface costimulatory molecules CD80, CD86 expression, and inhibited DC synthesis of IL-1α, IL-6, TNF-α. Conclusion IL-37 can inhibit LPS-stimulated DC activation by decreasing the expression of costimulatory molecules and inflammatory cytokines.