IL-12 and TNF-α production by dendritic cells stimulated with Schistosoma mansoni schistosomula tegument is TLR4-and MyD88-dependent
IL-12 and TNF-α production by dendritic cells stimulated with Schistosoma mansoni schistosomula tegument is TLR4-and MyD88-dependent
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DOI：
10.1016/j.imlet.2009.06.004
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发表时间：
2009-06-30
影响因子：
4.4
通讯作者：
Fonseca, Cristina T.
中科院分区：
文献类型：
--
作者：
Duraes, Fernanda V.;Carvalho, Natalia B.;Fonseca, Cristina T.
曼氏血吸虫童虫是最易受宿主免疫系统攻击的寄生虫。血吸虫被膜是一种独特的双膜结构，与宿主的营养和免疫逃避有关，宿主与寄生虫之间存在着复杂的相互作用。在此，我们已经证明了短体皮层（Smteg）激活树突状细胞以产生IL-12 p40、TNF-α，并且还上调共刺激分子CD 40和CD 86。此外，使用来自MyD 88-、TLR 2-、TLR 4-和TLR 9-缺陷小鼠的DC，我们已经表明Smteg激活DC产生IL-12和TNF-α的能力涉及TLR 4/Smteg相互作用和MyD 88信号通路。最后，我们的研究结果使我们得出结论，TLR 4是一个关键的受体参与Smteg诱导的促炎细胞因子。(C)2009爱思唯尔有限公司版权所有。
Schistosoma mansoni schistosomula are the most susceptible parasite life stage to host immune system attack. Complex host-parasite interactions take place on Schistosoma tegument, which is a unique double membrane structure involved in nutrition and immune evasion. Herein, we have demonstrated that schistosomula tegument (Smteg) activates Dendritic cells to produce IL-12p40, TNF-alpha and also to upregulate the co-stimulatory molecules CD40 and CD86. Moreover, using DCs derived from MyD88-, TLR2-, TLR4- and TLR9-deficient mice we have shown that the ability of Smteg to activate DCs to produce IL-12 and TNF-a involves TLR4/Smteg interaction and MyD88 signaling pathway. Finally, our findings lead us to conclude that TLR4 is a key receptor involved in Smteg induction of pro-inflammatory cytokines. (C) 2009 Elsevier B.V. All rights reserved.