KIR2DL2 inhibitory pathway enhances Th17 cytokine secretion by NK cells in response to herpesvirus infection in multiple sclerosis patients

被引:16
|
作者
Rizzo, Roberta [1 ]
Bortolotti, Dania [1 ]
Fainardi, Enrico [2 ]
Gentili, Valentina [1 ]
Bolzani, Silvia [1 ]
Baldi, Eleonora [3 ]
Casetta, Ilaria [4 ]
Granieri, Enrico [4 ]
Rotola, Antonella [1 ]
Furlan, Roberto [5 ]
Di Luca, Dario [1 ]
机构
[1] Univ Ferrara, Sect Microbiol & Med Genet, Dept Med Sci, Via Luigi Borsari 46, I-44121 Ferrara, Italy
[2] Azienda Osped Univ, Dept Neurosci & Rehabil, Neuroradiol Unit, Ferrara, Italy
[3] Azienda Osped Univ, Dept Neurosci & Rehabil, Neurol Unit, Ferrara, Italy
[4] Univ Ferrara, Dept Biomed & Specialist Surg Sci, Neurol Sect, I-44100 Ferrara, Italy
[5] Ist Sci San Raffaele, Div Neurosci, INSPE, I-20132 Milan, Italy
关键词
NK cells; Inhibitory receptor; Host/pathogens interactions; Herpesvirus; Th17; VIRUS-INFECTION; KILLER; RECEPTOR; MOLECULES; SUBSETS; CLONES;
D O I
10.1016/j.jneuroim.2016.03.007
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
We have previously demonstrated that multiple sclerosis (MS) patients with KIR2DL2 expression on Natural killer (NK) cells are more susceptible to herpes simplex virus 1 (HSV-1) infection. We explored cytokine expression by NK cells during HSV-1 infection in association with KIR2DL2 expression. MS KIR2DL2(+) NK cells failed to control HSV-1 infection and secreted high levels of Th17 cytokines, while MS KIR2DL2(-) NK cells released Th1 cytokines, mainly IFN-gamma. Our data showed, for the first time, a peculiar Th17 cytokine secretion by MS KIR2DL2(+) NK cells in the presence of HSV-1 infection, that could be implicated in MS pathogenesis. (C) 2016 Elsevier B.V. All rights reserved.
引用
收藏
页码:1 / 5
页数:5
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