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

机译:共生真菌和C型凝集素受体的Dectin-1影响结肠炎之间的相互作用

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摘要

The intestinal microflora, typically equated with bacteria, influences diseases such as obesity and inflammatory bowel disease (IBD). 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 t 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 novel 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.
机译:肠道微氟氯,通常等同于细菌,影响肥胖和炎症性肠病(IBD)等疾病。在这里,我们表明哺乳动物肠道含有丰富的真菌群落,通过先天免疫受体蛋白-1与免疫系统相互作用。缺乏Dectin-1的小鼠表现出增加的易感性T化学诱导的结肠炎,这是对土着真菌的反应改变的结果。在人类中,我们鉴定了与溃疡性结肠炎的严重形式强烈连接的Dectin-1(CLEC7A)中的多态性。我们的研究结果一起揭示了肠道(“骨髓型”)中的新型真核真菌群落,与细菌共存并大大扩大了与肠免疫系统相互作用以影响健康和疾病的生物体的曲目。

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