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      Interactions between commensal fungi and the C-type lectin receptor Dectin-1 influence colitis.

      Science (New York, N.Y.)

      Animals, Antibodies, Fungal, blood, Candida tropicalis, immunology, isolation & purification, pathogenicity, physiology, Colitis, Ulcerative, chemically induced, microbiology, Colon, Colony Count, Microbial, Dextran Sulfate, Disease Susceptibility, Female, Fungi, classification, Haplotypes, Humans, Immunity, Innate, Immunity, Mucosal, Intestinal Mucosa, Intestines, Lectins, C-Type, deficiency, genetics, metabolism, Metagenome, Mice, Mice, Inbred C57BL, Polymorphism, Single Nucleotide

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          Abstract

          The intestinal microflora, typically equated with bacteria, influences diseases such as obesity and inflammatory bowel disease. Here, we show that the mammalian gut contains a rich fungal community that interacts with the immune system through the innate immune receptor Dectin-1. Mice lacking Dectin-1 exhibited increased susceptibility to chemically induced colitis, which was the result of altered responses to indigenous fungi. In humans, we identified a polymorphism in the gene for Dectin-1 (CLEC7A) that is strongly linked to a severe form of ulcerative colitis. Together, our findings reveal a eukaryotic fungal community in the gut (the "mycobiome") that coexists with bacteria and substantially expands the repertoire of organisms interacting with the intestinal immune system to influence health and disease.

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          Author and article information

          Journal
          22674328
          3432565
          10.1126/science.1221789

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