| Literature DB >> 27736647 |
Alon Vitenshtein1, Yoav Charpak-Amikam1, Rachel Yamin1, Yoav Bauman1, Batya Isaacson1, Natan Stein1, Orit Berhani1, Liat Dassa1, Moriya Gamliel1, Chamutal Gur1, Ariella Glasner1, Carlos Gomez2, Ronen Ben-Ami3, Nir Osherov4, Brendan P Cormack5, Ofer Mandelboim6.
Abstract
Natural killer (NK) cells form an important arm of the innate immune system and function to combat a wide range of invading pathogens, ranging from viruses to bacteria. However, the means by which NK cells accomplish recognition of pathogens with a limited repertoire of receptors remain largely unknown. In the current study, we describe the recognition of an emerging fungal pathogen, Candida glabrata, by the human NK cytotoxic receptor NKp46 and its mouse ortholog, NCR1. Using NCR1 knockout mice, we observed that this receptor-mediated recognition was crucial for controlling C. glabrata infection in vitro and in vivo. Finally, we delineated the fungal ligands to be the C. glabrata adhesins Epa1, Epa6, and Epa7 and demonstrated that clearance of systemic C. glabrata infections in vivo depends on their recognition by NCR1. As NKp46 and NCR1 have been previously shown to bind viral adhesion receptors, we speculate that NKp46/NCR1 may be a novel type of pattern recognition receptor.Entities:
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Year: 2016 PMID： 27736647 PMCID： PMC5492882 DOI： 10.1016/j.chom.2016.09.008
Source DB: PubMed Journal: Cell Host Microbe ISSN： 1931-3128 Impact factor: 21.023