中文摘要：

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。

英文摘要：

To investigate the role of TLR2 in B cell activation by tumor derived-autophagosomes（DRs）, Bcells selected from spleen of mice using anti-CD43 dynabeads were incubated with TLR2 antibody（0, 3, 10, 30 μg/ml）,and then stimulated with DRs. At the 3^rdday, the expression of MHCⅡ and costimulatory molecule CD86 weredetected by flow cytometry, and the secretion of IL-6 and IL-10 in the supernatant were tested by ELISA. At the 7-（th） day, Ig M in the supernatant were tested by ELISA. Data showed that DRs barely up-regulated the expression of I-Aband CD86 on TLR2 antibody blocked-B cells, and the secretion of IL-6, IL-10 and Ig M of TLR2 antibodyblocked-B cells were significantly decreased when compared with unblocked-B cells. Therefore, our resultsdocument that TLR2 on B cell has an important effect on B cells activation induced by DRs.