Open AccessKIR2DL2 overexpression influences NK cell response to CpG
Author(s) -
Daria Bortolotti,
Antonella Rotola,
Di Luca Dario,
Rizzo Roberta
Publication year - 2013
Publication title -
frontiers in immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.646
H-Index - 124
ISSN - 1664-3224
DOI - 10.3389/conf.fimmu.2013.02.00130
Subject(s) - tlr9 , cpg site , biology , immunology , interleukin 21 , innate immune system , janus kinase 3 , microbiology and biotechnology , immune system , t cell , gene expression , gene , dna methylation , genetics
NK cells are innate effectors towards viral infections, sensing viral unmethylated CpG motifs (CpG-ODN) through TLR9. NK cell activation is controlled by killer-cell inhibitory and activating receptors\ud(KIR, KAR). Rizzo et al. [J Neuroimmunol 2012] reported that a 40% Multiple Sclerosis (MS) patients were unable to counteract herpesvirus infection after in vitro treatment of NK cells with CpGODN.\udThese NK cells showed an increased expression of the inhibitory receptor KIR2DL2 and its ligand HLA-C1, responsible for the reduced NK cell activation. On the basis of previous results that\udreported the role of KIR3DL2 in CpG-ODN binding [Sivori et al., Blood 2010], we evaluate the way of uptake of CpG-ODN in NK cell lines and its effect on KIRs expression and NK activity status. Our\uddata confirm the role of KIR3DL2 in CpG-ODN uptake and we observed, for the first time, the induction od KIR2DL2 that reduced NK citotoxic activity towards HLA-C1+ target cells. We showed that\udthis modulation via KIR3DL2-CpG-ODN was mediated by specific transcription factors and could explain the KIR2DL2+ NK cell unresponsivness to viral infection after CpG-ODN treatment