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目的:观察日本血吸虫可溶性虫卵抗原(SEA)是否能够诱导小鼠B细胞活化及其机制。方法:SEA和脂多糖(LPS)分别体外刺激小鼠脾脏CD19+B细胞,72 h后用流式细胞术分别检测B细胞表面CD80、CD86及CD40的表达和B细胞细胞周期的改变;用荧光染料CFSE分裂法检测B细胞增殖;用ELISA法检测培养上清中白介素(IL-)10、IL-6、γ干扰素(IFN-γ)和转化生长因子β(TGF-β)的水平。同时利用ERK、JNK、p38MAPK和NF-κB信号转导抑制剂检测B细胞分泌细胞因子水平的变化。结果:SEA与LPS组可以活化小鼠脾脏CD19+B细胞,使其表面高表达CD80、CD86和CD40;同时诱导S/G2期的B细胞比例显著增加,SEA可以诱导B细胞增殖。SEA与LPS能刺激脾脏CD19+B细胞分泌高水平的IL-10、IL-6。分别阻断NF-κB、ERK、JNK和p38MAPK信号转导通路后可以抑制B细胞IL-10和IL-6的分泌。结论:SEA可以上调小鼠脾脏B细胞表面共刺激分子表达、促进其增殖。同时,SEA可以通过NF-κB、ERK、JNK和p38MAPK信号转导通路刺激小鼠B细胞分泌细胞因子。
Objective: To observe whether Schistosoma japonicum soluble egg antigen (SEA) can induce the activation of mouse B cells and its mechanism. Methods: Splenic CD19 + B cells were stimulated with SEA and lipopolysaccharide (LPS) respectively. After 72 h, the expression of CD80, CD86 and CD40 and the cell cycle of B cells were detected by flow cytometry. Dye CFSE cleavage method was used to detect the proliferation of B cells. The levels of IL-10, IL-6, IFN-γ and TGF-β in culture supernatants were detected by ELISA. At the same time, ERK, JNK, p38MAPK and NF-κB signal transduction inhibitors were used to detect the changes of cytokines secreted by B cells. Results: The splenic CD19 + B cells were activated in SEA and LPS groups, and the expression of CD80, CD86 and CD40 was highly expressed on the surface of spleen cells. The percentage of B cells in S / G2 phase was significantly increased, and SEA induced the proliferation of B cells. SEA and LPS stimulate splenic CD19 + B cells to secrete high levels of IL-10 and IL-6. Blocking NF-κB, ERK, JNK and p38MAPK signal transduction pathway can inhibit the secretion of IL-10 and IL-6 in B cells. Conclusion: SEA can up-regulate the expression of costimulatory molecules on the surface of B lymphocytes in mice spleen and promote its proliferation. Meanwhile, SEA can stimulate mouse B cells to secrete cytokines through NF-κB, ERK, JNK and p38MAPK signal transduction pathways.