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为研究B细胞表面TLR2在B细胞交叉提呈肿瘤来源自噬小体(tumor derived-autophagosome,DR)抗原诱导效应T细胞再活化过程中的作用,DR经淋巴结注射方式免疫C57BL/6小鼠,收获免疫小鼠的淋巴结细胞作为效应T细胞;以负载DR的C57BL/6、TLR2~(-/-)和MyD88~(-/-)及TLR2抗体封闭的小鼠脾脏B细胞作为pAPC。DR分别与分离纯化的WT C57BL/6、TLR2~(-/-)和MyD88~(-/-)及TLR2抗体封闭后的小鼠B细胞共孵育,然后与免疫小鼠CD4~+T和CD8~+T细胞共孵育,流式细胞术及ELISA法检测IFN-γ的分泌水平。结果显示,与WT C57BL/6小鼠B细胞组相比,负载DR的TLR2~(-/-)B细胞和MyD88~(-/-)B细胞及TLR2抗体封闭的B细胞活化效应CD8~+T和CD4~+T细胞产生的IFN-γ水平显著降低。以上结果提示B细胞交叉提呈DR抗原、诱导效应T细胞活化依赖于TLR2/MyD88信号通路。
In order to investigate the role of TLR2 on the reactivation of T cells induced by B cell cross-presenting tumor derived-autophagosome (DR) antigen, C57BL / 6 mice were immunized by lymph node injection. The lymphocytes from the immunized mice were harvested as effector T cells. The splenic B cells from mice bearing C57BL / 6, TLR2 ~ (- / -) and MyD88 ~ (- / -) and TLR2- DR were separately incubated with B cells isolated from mice with isolated and purified WT C57BL / 6, TLR2 ~ (- / -) and MyD88 ~ (- / -) and TLR2 antibodies and then with CD4 ~ + T and CD8 ~ + T cells were co-incubated with flow cytometry and ELISA to detect IFN-γ secretion levels. The results showed that compared with WT C57BL / 6 mice, B cell activation induced by TLR2 ~ (- / -) B cells and MyD88 ~ (- / -) B cells and TLR2- T and CD4 ~ + T cells produced IFN-γ levels were significantly lower. These results suggest that B cells cross-presentation of DR antigen, induction of effector T cell activation depends on the TLR2 / MyD88 signaling pathway.