IL-37b通过抑制树突状细胞相关的免疫应答缓解感染性休克

发布时间：2018-04-13 01:16

本文选题：IL-b + 纯化　；参考：《中国比较医学杂志》2017年11期

【摘要】：目的表达IL-37b重组蛋白,研究其在调节机体免疫应答方面的作用机制。方法构建原核表达载体p ET28/IL-37b,诱导表达的IL-37b重组蛋白由Ni~(2+)-NTA凝胶进行纯化。将IL-37b作用于C57BL/6 J小鼠,注射LPS诱导感染性休克,检测小鼠血清中IL-1β、IL-6、IFN-γ的表达水平。分离并培养小鼠树突状细胞,用IL-37b处理,经LPS诱导活化,检测细胞表面CD40、CD80、MHCII等标志物分子表达情况,以及培养上清中IL-1β、IL-10、IL-12、TNF-α的表达水平。分离小鼠CD4~+T细胞,检测IL-37b对LPS诱导的T细胞培养上清中IFN-γ、TNF-α、IL-10的抑制作用。结果IL-37b能够降低感染性休克的小鼠血清中促炎性细胞因子的表达;并抑制小鼠树突状细胞共刺激分子和促炎性细胞因子的表达,以及CD4~+T细胞表达促炎性细胞因子。结论纯化的IL-37b具备生物学活性,能够通过抑制树突状细胞活化及相关的T细胞免疫应答缓解机体感染性休克。
[Abstract]:Objective to express recombinant IL-37b protein and study its mechanism in regulating immune response.Methods the prokaryotic expression vector pET28 / IL-37b was constructed and the IL-37b recombinant protein was purified by Ni~(2-NTA gel.IL-37b was injected into C57BL/6 J mice to induce septic shock, and the expression level of IL-1 尾 -IL-6 IFN- 纬 in serum of mice was detected.Mouse dendritic cells were isolated and cultured, treated with IL-37b, and activated by LPS. The expression of CD40, CD80, MHCII and the expression of IL-1 尾 -IL-10 and IL-12 TNF- 伪 on the cell surface were detected.Mouse CD4T cells were isolated and the inhibitory effect of IL-37b on IFN- 纬 -TNF- 伪 IL-10 in the supernatant of T cell culture induced by LPS was detected.Results IL-37b could decrease the expression of pro-inflammatory cytokines in serum of mice with septic shock, inhibit the expression of costimulatory molecules and pro-inflammatory cytokines in dendritic cells, and the expression of pro-inflammatory cytokines in CD4T cells.Conclusion the purified IL-37b has biological activity and can relieve septic shock by inhibiting dendritic cell activation and T cell immune response.
【作者单位】：中国医学科学院医学实验动物研究所北京协和医学院比较医学中心;定西市中医院骨伤一科;
【基金】：中国医学科学院医学与健康科技创新工程-重大协同创新项目-协同创新团队资助(编号:2016-I2M-3-019)
【分类号】：R392

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