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人类原发性髓样树突状细胞通过C型凝集素受体Dectin-1与机会性真菌病原体烟曲霉相互作用。

Human primary myeloid dendritic cells interact with the opportunistic fungal pathogen Aspergillus fumigatus via the C-type lectin receptor Dectin-1.

作者信息

Hefter Maike, Lother Jasmin, Weiß Esther, Schmitt Anna Lena, Fliesser Mirjam, Einsele Hermann, Loeffler Juergen

机构信息

Medizinische Klinik und Poliklinik II, University Hospital Wuerzburg, Wuerzburg, Germany.

出版信息

Med Mycol. 2017 Jul 1;55(5):573-578. doi: 10.1093/mmy/myw105.

DOI:10.1093/mmy/myw105
PMID:28873980
Abstract

Aspergillus fumigatus is an opportunistic fungal pathogen causing detrimental infections in immunocompromised individuals. Dendritic cells (DCs) are potent antigen-presenting cells and recognize the A. fumigatus cell wall component β-1,3 glucan via Dectin-1, followed by DC maturation and cytokine release. Here, we demonstrate that human primary myeloid DCs (mDCs) interact with different morphotypes of A. fumigatus. Dectin-1 is expressed on mDCs and is down-regulated after contact with A. fumigatus, indicating that mDCs recognize A. fumigatus via this receptor. Blocking of Dectin-1, followed by stimulation with depleted zymosan diminished the up-regulation of the T-cell co-stimulatory molecules CD40, CD80, HLA-DR and CCR7 on mDCs and led to decreased release of the cytokines TNF-α, IL-8, IL-1β and IL-10.

摘要

烟曲霉是一种机会性真菌病原体,可在免疫功能低下的个体中引起有害感染。树突状细胞(DCs)是强大的抗原呈递细胞,可通过Dectin-1识别烟曲霉细胞壁成分β-1,3-葡聚糖,随后DC成熟并释放细胞因子。在此,我们证明人类原代髓样DCs(mDCs)与烟曲霉的不同形态型相互作用。Dectin-1在mDCs上表达,与烟曲霉接触后下调,表明mDCs通过该受体识别烟曲霉。阻断Dectin-1,然后用脱毒酵母聚糖刺激,可减少mDCs上T细胞共刺激分子CD40、CD80、HLA-DR和CCR7的上调,并导致细胞因子TNF-α、IL-8、IL-1β和IL-10的释放减少。

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