Abstract
Dectin-1 is an innate antifungal C-type lectin receptor necessary for protective antifungal immunity. We recently discovered that Dectin-1 is involved in controlling fungal infections of the gastrointestinal (GI) tract, but how this C-type lectin receptor mediates these activities is unknown. Here, we show that Dectin-1 is essential for driving fungal-specific CD4(+) T-cell responses in the GI tract. Loss of Dectin-1 resulted in abrogated dendritic cell responses in the mesenteric lymph nodes (mLNs) and defective T-cell co-stimulation, causing substantial increases in CD4(+) T-cell apoptosis and reductions in the cellularity of GI-associated lymphoid tissues. CD8(+) T-cell responses were unaffected by Dectin-1 deficiency. These functions of Dectin-1 have significant implications for our understanding of intestinal immunity and susceptibility to fungal infections.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adoptive Transfer
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Animals
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Apoptosis / immunology
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CD4-Positive T-Lymphocytes / immunology*
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CD4-Positive T-Lymphocytes / microbiology
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CD4-Positive T-Lymphocytes / pathology
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CD4-Positive T-Lymphocytes / transplantation
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CD8-Positive T-Lymphocytes / immunology*
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CD8-Positive T-Lymphocytes / microbiology
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CD8-Positive T-Lymphocytes / pathology
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Candida albicans / immunology*
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Candidiasis / genetics
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Candidiasis / immunology*
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Candidiasis / microbiology
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Candidiasis / pathology
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Cell Survival / immunology
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Female
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Gastrointestinal Tract / immunology*
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Gastrointestinal Tract / microbiology
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Gastrointestinal Tract / pathology
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Gene Expression
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Lectins, C-Type / deficiency
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Lectins, C-Type / genetics
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Lectins, C-Type / immunology*
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Lymph Nodes / immunology
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Lymph Nodes / microbiology
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Lymph Nodes / pathology
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Lymphocyte Activation
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Mesentery / immunology
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Mesentery / microbiology
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Mesentery / pathology
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Mice
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Mice, Inbred C57BL
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Mice, Knockout