期刊
MUCOSAL IMMUNOLOGY
卷 9, 期 2, 页码 492-502出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/mi.2015.79
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资金
- Medical Research Council
- Wellcome Trust [086558, 102705, 97377]
- University of Aberdeen
- Medical Research Council [MR/J004820/1, 980074, MR/N006364/1] Funding Source: researchfish
- Wellcome Trust [102705/Z/13/Z] Funding Source: researchfish
- MRC [MR/N006364/1, MR/J004820/1] Funding Source: UKRI
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.
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