Abstract
Schistosomes are helminth parasites that display a dual impact on the immune system of their hosts. Although the larval stage, also known as schistosomulum, appears to subvert the host defenses, the egg stage induces strong inflammatory reactions. Given the pivotal role of dendritic cells (DC) in initiating and regulating immune responses, we compared the distinct transcriptional programs induced in immature mouse DC by S. mansoni eggs or schistosomula. Although SLA abrogated the transcription of many genes implicated in DC functions, eggs caused myeloid DC to produce IFN-beta. Autocrine/paracrine signaling through the type I IFN receptor in response to eggs was necessary for the induction of known IFN-responsive genes and enhanced the synthesis of key inflammatory products. Taken as a whole, our data provide molecular insights into the immune evasion mechanism of schistosomula and suggest an unexpected role for type I IFN in the innate response to helminth eggs.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Autocrine Communication / genetics
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Autocrine Communication / immunology
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Cell Line
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Dendritic Cells / immunology*
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Dendritic Cells / metabolism
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Dendritic Cells / parasitology
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Dendritic Cells / pathology
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Gene Expression Profiling
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Inflammation / genetics
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Inflammation / immunology*
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Inflammation / parasitology
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Interferon-beta / biosynthesis
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Interferon-beta / physiology*
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Larva / growth & development
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Larva / immunology
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Membrane Proteins
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Mice
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Mice, Knockout
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Multigene Family / immunology
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Myeloid Cells / immunology*
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Myeloid Cells / parasitology
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Myeloid Cells / pathology
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Oligonucleotide Array Sequence Analysis
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Ovum / immunology*
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Paracrine Communication / genetics
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Paracrine Communication / immunology
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Receptor, Interferon alpha-beta
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Receptors, Interferon / biosynthesis
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Receptors, Interferon / deficiency
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Receptors, Interferon / physiology
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Schistosoma mansoni / growth & development
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Schistosoma mansoni / immunology*
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Signal Transduction / genetics
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Signal Transduction / immunology*
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Transcription, Genetic / immunology
Substances
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Membrane Proteins
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Receptors, Interferon
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Receptor, Interferon alpha-beta
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Interferon-beta