期刊
SCIENCE
卷 336, 期 6080, 页码 489-493出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1219328
关键词
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资金
- NIH [DK44319, DK51362, DK53056, DK88199, AI090102]
- Crohn's Colitis Foundation of America
- Harvard Digestive Diseases Center [DK034854]
- Medizinausschuss Schleswig-Holstein, German Ministry of Education Research through the National Genome Research Network
- Medical Faculty, Kiel
- Deutsche Forschungsgemeinschaft (DFG) [OL 324/1-1, SZ 814/1-1, 814/4-1]
- DFG Excellence Cluster Inflammation at Interfaces
Exposure to microbes during early childhood is associated with protection from immune-mediated diseases such as inflammatory bowel disease (IBD) and asthma. Here, we show that in germ-free (GF) mice, invariant natural killer T (iNKT) cells accumulate in the colonic lamina propria and lung, resulting in increased morbidity in models of IBD and allergic asthma as compared with that of specific pathogen-free mice. This was associated with increased intestinal and pulmonary expression of the chemokine ligand CXCL16, which was associated with increased mucosal iNKT cells. Colonization of neonatal-but not adult-GF mice with a conventional microbiota protected the animals from mucosal iNKT accumulation and related pathology. These results indicate that age-sensitive contact with commensal microbes is critical for establishing mucosal iNKT cell tolerance to later environmental exposures.
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