B细胞表面TLR2受体在肿瘤来源自噬小体活化B细胞过程中的作用

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目的研究B细胞表面TLR2受体在肿瘤来源自噬小体活化B细胞过程中的作用。方法抗CD43磁珠分选法分离小鼠脾脏B细胞,用不同质量浓度TLR2抗体(0、3、10、30μg/ml)与B细胞共孵育,再用肿瘤来源自噬小体(DRs)刺激B细胞72 h,流式细胞术检测B细胞表面MHCⅡ类分子及共刺激分子CD86的表达情况;第3天收取上清ELISA检测细胞培养上清中IL-6和IL-10的表达;第7天收取上清液,ELISA检测细胞培养上清液中Ig M的表达。结果与未预处理的B细胞组相比,DRs活化TLR2抗体封闭的B细胞组上调B细胞表面MHCⅡ类分子和CD86表达的作用明显降低;DRs刺激TLR2抗体封闭B细胞组分泌IL-6和IL-10的水平显著降低;DRs刺激TLR2抗体封闭的B细胞产生Ig M水平显著低于未预处理的B细胞组。结论 B细胞的TLR2受体在DRs诱导B细胞活化、分泌细胞因子及产生Ig M过程中发挥了重要作用。 Objective To investigate the role of TLR2 receptor on B cell surface in the activation of B cells by phagocytes. Methods B cells were isolated from splenic lymphocytes of mice by anti-CD43 magnetic bead sorting method and incubated with B lymphocytes with different concentrations of TLR2 antibody (0, 3, 10, 30μg / ml) and then stimulated with tumor-derived phage B cells for 72 h, the expression of MHC class II molecules and costimulatory molecules CD86 on B cells were detected by flow cytometry; the supernatant ELISA was performed on the third day to detect the expression of IL-6 and IL-10 in the cell culture supernatant; The supernatant was collected and the IgM expression in cell culture supernatants was detected by ELISA. Results Compared with non-pretreated B cells, the expression of MHC class II molecules and CD86 on the surface of B cells was significantly decreased in DRG-activated TLR2-blocking B cells. DRs stimulated TLR2-blocking B cells to secrete IL-6 and IL- -10 levels were significantly decreased; IgM levels in B cells stimulated by DRs stimulated by TLR2 antibody were significantly lower than those in untreated B cells. Conclusion The B cell TLR2 receptor plays an important role in the activation of B cells induced by DRs, the secretion of cytokines and the production of IgM.
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