乳凝集素通过ERK、p38 MAPK通路调节未成熟树突状细胞分泌IL-12和IL-10的研究

发布时间：2018-04-25 02:06

本文选题：乳凝集素 + ERK　；参考：《上海交通大学学报(医学版)》2013年07期

【摘要】：目的探讨乳凝集素通过ERK、p38 MAPK信号通路对未成熟树突状细胞(iDCs)分泌白介素(IL)-12和IL-10的影响。方法脐带血中分离得到单核细胞,加入重组人粒细胞巨噬细胞集落刺激因子(50 ng/mL)和重组人白介素-4(10 ng/mL),同时按照不同组合加入乳凝集素(10μg/mL)和信号通路阻滞剂,诱导分化为iDCs。分组如下:①对照组;②乳凝集素组;③ERK通路阻滞组;④ERK通路阻滞剂+乳凝集素组;⑤p38MAPK通路阻滞组;⑥p38MAPK通路阻滞剂+乳凝集素组;⑦JNK通路阻滞组;⑧JNK通路阻滞剂+乳凝集素组。采用Western blotting检测ERK、JNK、p38MAPK蛋白磷酸化水平,ELISA法检测iDCs分泌IL-12和IL-10的变化。结果与对照组比较,乳凝集素组ERK蛋白磷酸化水平升高(P0.05),p38 MAPK蛋白磷酸化水平降低(P0.05),JNK蛋白磷酸化水平无明显差异(P0.05),IL-12和IL-10的分泌量显著降低(P0.05),IL-12/IL-10比值显著升高(P0.05)。ERK通路阻滞组和ERK通路阻滞剂+乳凝集素组中ERK蛋白磷酸化水平几乎为零;ERK阻滞剂+乳凝集素组IL-12和IL-10的分泌量显著高于乳凝集素组(P0.05),IL-12/IL-10比值显著低于乳凝集素组(P0.05)。p38 MAPK通路阻滞组和p38 MAPK通路阻滞剂+乳凝集素组中p38 MAPK蛋白磷酸化水平几乎为零;p38 MAPK通路阻滞剂+乳凝集素组IL-12和IL-10的分泌量显著低于乳凝集素组(P0.05),IL-12/IL-10比值显著高于乳凝集素组(P0.05)。结论乳凝集素可能通过激活ERK通路的活化及抑制p38MAPK通路的活化调节iDCs分泌IL-10和IL-12。
[Abstract]:Objective to investigate the effect of milk agglutinin on the secretion of interleukins (IL) -12 and IL-10 by ERK, p38 MAPK signaling pathway in immature dendritic cells (iDCs). Methods mononuclear cells were isolated from umbilical cord blood and added to the recombinant human granulocyte macrophage colony stimulating factor (50 ng/mL) and recombinant human interleukin -4 (10 ng/mL), and were added to different combinations according to different combinations. Milk agglutinin (10 g/mL) and signal pathway blockers were induced to differentiate into iDCs. groups as follows: (1) control group; (2) group of milk agglutinin; (3) ERK pathway block group; (4) ERK pathway blocker + lectin group; (5) p38MAPK pathway block group; (6) p38MAPK pathway blocker + lectin group; JNK pathway block group; JNK pathway blocker + lectin group Western blotting was used to detect the phosphorylation level of ERK, JNK, p38MAPK protein. ELISA method was used to detect the changes of IL-12 and IL-10 in iDCs. Compared with the control group, the phosphorylation level of ERK protein in the milk agglutinin group increased (P0.05), the phosphorylation level of the p38 protein protein decreased, and there was no significant difference in the phosphorylation level of the protein. The secretion was significantly decreased (P0.05), the ratio of IL-12/IL-10 increased significantly (P0.05) in the.ERK pathway block group and the ERK protein phosphorylation level in the ERK pathway blocker + lectin group was almost zero, and the secretion of IL-12 and IL-10 in the ERK blocker + lectin group was significantly higher than that in the milk agglutinin group (P0.05), and the IL-12/IL-10 ratio was significantly lower than the lectin group (P0.05). The level of p38 MAPK protein phosphorylation in the.P38 MAPK pathway block group and the p38 MAPK pathway blocker + lectin group was almost zero, and the secretion of IL-12 and IL-10 in the p38 MAPK pathway blocker + lectin group was significantly lower than the milk agglutinin group (P0.05), and the IL-12/IL-10 ratio was significantly higher than that of the milk agglutinin group. Conclusion the milk agglutinin may be activated by the activation of the milk agglutinin. Activation of ERK pathway and inhibition of activation of p38MAPK pathway regulate iDCs secretion of IL-10 and IL-12.

【作者单位】：上海交通大学医学院附属新华医院新生儿科;
【基金】：上海市科委基金(10411966100)~~
【分类号】：R363

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