期刊
NATURE IMMUNOLOGY
卷 8, 期 1, 页码 31-38出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni1408
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- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL080317] Funding Source: NIH RePORTER
- Biotechnology and Biological Sciences Research Council [BBS/B/10331] Funding Source: Medline
- NHLBI NIH HHS [1R01HL080317, R01 HL080317] Funding Source: Medline
- Wellcome Trust [055109, 071467, 070018, 072420, 070579] Funding Source: Medline
beta-Glucan is one of the most abundant polysaccharides in fungal pathogens, yet its importance in antifungal immunity is unclear. Here we show that deficiency of dectin-1, the myeloid receptor for beta-glucan, rendered mice susceptible to infection with Candida albicans. Dectin-1-deficient leukocytes demonstrated significantly impaired responses to fungi even in the presence of opsonins. Impaired leukocyte responses were manifested in vivo by reduced inflammatory cell recruitment after fungal infection, resulting in substantially increased fungal burdens and enhanced fungal dissemination. Our results establish a fundamental function for beta-glucan recognition by dectin-1 in antifungal immunity and demonstrate a signaling non-Toll-like pattern-recognition receptor required for the induction of protective immune responses.
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