论文部分内容阅读
目的:运用EμSR-BCL10转基因小鼠模型研究BCL10高表达致黏膜相关淋巴组织(MALT)淋巴瘤的分子机制。方法:用IgM+/CD21high/CD23low荧光标记的抗体染色后进行流式细胞仪分析MZ B细胞;用CD43和CD23磁珠抗体双阴性分离方法获得MZ B细胞并用于体外增殖刺激实验;使用anti-IgM体内注射法研究BCL10体内抗凋亡。结果:MZB细胞增生与BCL10蛋白表达水平存在量效关系。细胞增殖实验结果显示,anti-IgM刺激时转基因小鼠的MZB细胞比FVB野生型小鼠对照增殖高2～5倍,但在LPS或PMA+Ionomycin刺激时,两者差异无统计学意义。同时anti-IgM体内注射能诱导FVB小鼠的MZ B细胞凋亡,但转基因小鼠的MZ B细胞不发生凋亡。结论:BCL10表达水平与MALT淋巴瘤的前体细胞-MZ B细胞的增生具有正相关的量效关系,其导致增生的机制是其位于BCR受体下游使MZ B细胞在BCR受到刺激时增殖增强并且不发生凋亡。
OBJECTIVE: To study the molecular mechanism of BCL10 overexpression in mucosal associated lymphoid tissue (MALT) lymphoma using EμSR-BCL10 transgenic mouse model. METHODS: MZ B cells were stained with IgM + / CD21high / CD23low fluorescently labeled antibody and MZ B cells by flow cytometry. MZ B cells were obtained by double-negative isolation of CD43 and CD23 beads antibody and used for in vitro proliferation stimulation experiments. Anti-IgM In vivo anti-apoptotic effect of BCL10 in vivo. Results: There was dose-response relationship between MZB cell proliferation and BCL10 protein expression. The results of cell proliferation assay showed that MZB cells in transgenic mice were 2 ~ 5 times more proliferative than those in FVB wild-type mice when stimulated with anti-IgM, but there was no significant difference between the two groups when stimulated with LPS or PMA + Ionomycin. At the same time, anti-IgM in vivo could induce MZ B cell apoptosis in FVB mice, but MZ B cells in transgenic mice did not undergo apoptosis. CONCLUSION: BCL10 expression is positively correlated with the proliferation of MZ B cells in MALT lymphoma. The mechanism of hyperplasia is that it is located in the downstream of BCR receptors and enhances the proliferation of MZ B cells when BCR is stimulated And no apoptosis occurred.