The secretions products from invading cercariae of S. japonicum (0–3hRP) restrain mouse dendritic cells to mature
The secretions products from invading cercariae of S. japonicum (0–3hRP) restrain mouse dendritic cells to mature
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DOI：
10.1007/s00436-011-2458-5
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发表时间：
2011
影响因子：
2
通讯作者：
Hejun Zhou;Xi Sun;Z. Lv;Yujuan Shen;Hui Peng;Lingling Yang;Huanquin Zheng;M. Fung;Jianping Cao;Zhongdao Wu
中科院分区：
文献类型：
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作者：
Hejun Zhou;Xi Sun;Z. Lv;Yujuan Shen;Hui Peng;Lingling Yang;Huanquin Zheng;M. Fung;Jianping Cao;Zhongdao Wu
血吸虫病是一种水源性传染病，主要由人类血吸虫引起，包括曼氏血吸虫（S. mansoni）和日本血吸虫（S. japonicum）。在受感染的宿主中，皮肤中的免疫事件似乎在确定随后的获得性免疫反应的类型和指导程度方面具有重要的启动作用。 S的先前研究。 Mansoni 表明，树突状细胞 (DC) 在被血吸虫幼虫释放的产物激活后会引发 Th2 反应（物质在转化后的前 3 小时内释放，0-3hRP）。因此，了解 0–3hRP 是否来自 S 是很有趣的。 japonicum 还可以激活 DC 并诱导 Th2 免疫反应。在这里，我们报告了 S 的 0–3hRP。日本血吸虫不能刺激骨髓源性树突状细胞（BM-DCs）的成熟，而尾蚴体制剂（SCAP）的可溶性抗原可诱导骨髓源性树突状细胞（BM-DCs）成熟，但0-3hRP可减弱这种成熟作用。此外，使用体外卵清蛋白肽限制性引发试验，用0-3hRP处理的DC未能诱导DO11.10转基因小鼠的CD4+T细胞比阴性对照组分泌更多的细胞因子，而用SCAP处理的DC上调IFN-γ和IL-17A的分泌，但下调IL-4。重要的是，用 0-3hRP 加 SCAP 处理的 BM-DC 诱导 BM-DC 选择性成熟，从而驱动 Th2 型极化反应。我们的体外结果与通过用卵清蛋白肽脉冲的不同刺激激活的 DC 接种 DO11.10 小鼠进行的体内研究结果一致。我们的数据表明，入侵尾蚴的分泌物。 japonicum(0–3hRP) 损害 DC 的成熟，这可能使寄生虫能够协商免疫识别和攻击。
Schistosomiasis is a water-borne infection caused mainly by human schistosomes includingSchistosoma mansoni(S. mansoni) andSchistosoma japonicum(S. japonicum). In the infected host, immune events in the skin appear to have an important initiating role in determining the type, and guiding the magnitude, of the ensuing acquired immune response. The previous studies ofS. mansonishowed that dendritic cells (DCs) prime Th2 response after activating with products released by schistosome larvae (material released in the first 3 h after transformation, 0–3hRP). Therefore, it is interesting to know whether 0–3hRP fromS. japonicumalso activate DC and induce Th2 immune response. Here, we report 0–3hRP ofS. japonicumfailed to stimulate the maturation of bone marrow-derived DCs (BM-DCs), while soluble antigen of the body of cercariae preparation (SCAP) induced BM-DCs to mature which can be weakened by 0–3hRP. Moreover, using an in vitro ovalbumin peptide-restricted priming assay, DCs treated with 0–3hRP failed to induce T cells to secrete more cytokines than the negative control group by CD4+T cells from DO11.10 transgenic mice, while DCs treated with SCAP upregulated secretions of IFN-γ and IL-17A, but downregulated IL-4. Importantly, BM-DCs treated with 0–3hRP plus SCAP induced BM-DCs selective mature which drive Th2-type polarized response. Our in vitro results agree with the findings of in vivo studies by inoculation of DO11.10 mice with different stimulus-activated DCs pulsed with ovalbumin peptide. Our data demonstrate that the secretions from invading cercariae ofS. japonicum(0–3hRP) impaired DCs to mature, which is potentially allowing the parasite to negotiate the immune recognition and attack.