Abstract
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 up-regulate 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-alpha 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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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B7-2 Antigen / immunology
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B7-2 Antigen / metabolism
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CD40 Antigens / immunology
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CD40 Antigens / metabolism
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Dendritic Cells / immunology*
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Host-Parasite Interactions / immunology*
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Interleukin-12 Subunit p40 / biosynthesis*
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Interleukin-12 Subunit p40 / immunology
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Lipopolysaccharides / pharmacology
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Myeloid Differentiation Factor 88 / genetics
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Myeloid Differentiation Factor 88 / immunology*
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Schistosoma mansoni / immunology*
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Signal Transduction / immunology
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Toll-Like Receptor 4 / genetics
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Toll-Like Receptor 4 / immunology*
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Tumor Necrosis Factor-alpha / biosynthesis*
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Tumor Necrosis Factor-alpha / immunology
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Up-Regulation / immunology
Substances
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B7-2 Antigen
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CD40 Antigens
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Interleukin-12 Subunit p40
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Lipopolysaccharides
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Myd88 protein, mouse
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Myeloid Differentiation Factor 88
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Toll-Like Receptor 4
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Tumor Necrosis Factor-alpha