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

Interactions between commensal fungi and the C-type lectin receptor Dectin-1 influence colitis.
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DOI:
10.1126/science.1221789
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发表时间:
2012-06-08
期刊:
Science (New York, N.Y.)
影响因子:
--
通讯作者:
Underhill DM
Underhill DM
中科院分区:
其他
文献类型:
--
作者:
Iliev ID;Funari VA;Taylor KD;Nguyen Q;Reyes CN;Strom SP;Brown J;Becker CA;Fleshner PR;Dubinsky M;Rotter JI;Wang HL;McGovern DP;Brown GD;Underhill DM

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肠道微生物菌群,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Dectin-1与免疫系统相互作用。缺乏Dectin-1的小鼠表现出对化学诱导的结肠炎的易感性增加,这是对本土真菌的反应改变的结果。在人类中,我们确定了Dectin-1(CLEC 7A)基因的多态性,该基因与严重形式的溃疡性结肠炎密切相关。总之,我们的研究结果揭示了肠道中一种新的真核真菌群落(“真菌群落”),它与细菌共存,并大大扩展了与肠道免疫系统相互作用的生物体的库,以影响健康和疾病。
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.
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