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杜克雷嗜血杆菌激活人类自然杀伤细胞的机制。

Mechanism of human natural killer cell activation by Haemophilus ducreyi.

作者信息

Li Wei, Janowicz Diane M, Fortney Kate R, Katz Barry P, Spinola Stanley M

机构信息

Department of Medicine, Center for Immunobiology, School of Medicine, Indiana University, Indianapolis, Indiana 46202, USA.

出版信息

J Infect Dis. 2009 Aug 15;200(4):590-8. doi: 10.1086/600123.

DOI:10.1086/600123
PMID:19572804
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2768539/
Abstract

The role of natural killer (NK) cells in the host response to Haemophilus ducreyi infection is unclear. In pustules obtained from infected human volunteers, there was an enrichment of CD56bright NK cells bearing the activation markers CD69 and HLA-DR, compared with peripheral blood. To study the mechanism by which H. ducreyi activated NK cells, we used peripheral blood mononuclear cells from uninfected volunteers. H. ducreyi activated NK cells only in the presence of antigen-presenting cells. H. ducreyi-infected monocytes and monocyte-derived macrophages activated NK cells in a contact- and interleukin-18 (IL-18)-dependent manner, whereas monocyte-derived dendritic cells induced NK activation through soluble IL-12. More lesional NK cells than peripheral blood NK cells produced IFN-gamma in response to IL-12 and IL-18. We conclude that NK cells are recruited to experimental lesions and likely are activated by infected macrophages and dendritic cells. IFN-gamma produced by lesional NK cells may facilitate phagocytosis of H. ducreyi.

摘要

自然杀伤(NK)细胞在宿主对杜克雷嗜血杆菌感染的反应中所起的作用尚不清楚。在从受感染的人类志愿者身上获取的脓疱中,与外周血相比,携带活化标记CD69和HLA - DR的CD56bright NK细胞有所富集。为了研究杜克雷嗜血杆菌激活NK细胞的机制,我们使用了未受感染志愿者的外周血单个核细胞。杜克雷嗜血杆菌仅在存在抗原呈递细胞的情况下激活NK细胞。感染杜克雷嗜血杆菌的单核细胞和单核细胞衍生的巨噬细胞以接触和白细胞介素18(IL - 18)依赖的方式激活NK细胞,而单核细胞衍生的树突状细胞则通过可溶性IL - 12诱导NK细胞活化。与外周血NK细胞相比,更多的病灶NK细胞在受到IL - 12和IL - 18刺激后产生γ干扰素。我们得出结论,NK细胞被募集到实验性病灶中,并且可能被感染的巨噬细胞和树突状细胞激活。病灶NK细胞产生的γ干扰素可能促进杜克雷嗜血杆菌的吞噬作用。

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A fibrinogen-binding lipoprotein contributes to the virulence of Haemophilus ducreyi in humans.一种纤维蛋白原结合脂蛋白有助于杜氏嗜血杆菌在人类中的致病性。
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IL-23 modulates CD56+/CD3- NK cell and CD56+/CD3+ NK-like T cell function differentially from IL-12.白细胞介素-23与白细胞介素-12不同,它对CD56+/CD3-自然杀伤细胞和CD56+/CD3+自然杀伤样T细胞功能的调节方式存在差异。
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