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Candida albicans-epithelial interactions and induction of mucosal innate immunity
被引:110
作者:
Naglik, Julian R.
[1
]
Koenig, Annika
[2
]
Hube, Bernhard
[2
,3
,4
]
Gaffen, Sarah L.
[5
]
机构:
[1] Kings Coll London, Inst Dent, Mucosal & Salivary Biol Div, London SE1 1UL, England
[2] Hans Krioell Inst, Dept Microbial Pathogen Mech, Leibniz Inst Nat Prod Res & Infect Biol, Jena, Germany
[3] Friedrich Schiller Univ, Jena, Germany
[4] Univ Hosp, Ctr Sepsis Control & Care, Jena, Germany
[5] Univ Pittsburgh, Div Rheumatol & Clin Immunol, Pittsburgh, PA 15261 USA
基金:
英国生物技术与生命科学研究理事会;
英国医学研究理事会;
关键词:
NEUTROPHIL EXTRACELLULAR TRAPS;
HOST-DEFENSE;
TRANSGLUTAMINASE SUBSTRATE;
GENE-EXPRESSION;
TH17;
CELLS;
VIRULENCE;
RESPONSES;
ADHESION;
ALS3;
INFLAMMASOME;
D O I:
10.1016/j.mib.2017.10.030
中图分类号:
Q93 [微生物学];
学科分类号:
071005 ;
100705 ;
摘要:
Candida albicans is a human fungal pathogen that causes millions of mucosal and life-threatening infections annually. C. albicans initially interacts with epithelial cells, resulting in fungal recognition and the formation of hyphae. Hypha formation is critical for host cell damage and immune activation, which are both driven by the secretion of Candidalysin, a recently discovered peptide toxin. Epithelial activation leads to the production of inflammatory mediators that recruit innate immune cells including neutrophils, macrophages and innate Type 17 cells, which together work with epithelial cells to clear the fungal infection. This review will focus on the recent discoveries that have advanced our understanding of C. albicans-epithelial interactions and the induction of mucosal innate immunity.
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页码:104 / 112
页数:9
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