Decreased interferon-γ production by NK cells from KIR haplotype B carriers in hepatitis C virus infection.

摘要: BACKGROUND AND AIMS Different population genetics studies showed that interactions between killer-cell immunoglobulin-like receptors (KIR) and HLA play a role in viral disease outcome, but functional correlates are missing. Building upon our previous work pointing to regulatory for KIR3DL1/DS1 hepatitis C virus (HCV) infection, we analysed whether its expression may affect natural killer (NK) cell function the presence or absence of principal ligand HLA-Bw4 KIR haplotype A B carriers, which characterized by different representation activating inhibitory KIRs. METHODS We performed class I genotypic analysis 54 healthy donors (HD) 50 HCV+ subjects examined NK cytokine secretion degranulation context KIR3DL1-HLA-Bw4 match stratified haplotype. RESULTS induced modulation, reflected reduced interferon (IFN)γ production patients compared HD. This impairment could be ascribed KIR3DS1 negative HCV-infected patient population, whose cells also significantly decreased proportion KIR3DL1. Haplotype increased with HD KIR-HLA-Bw4 this activity was associated phosphorylation signal transducer activator transcription (STAT) 1. CONCLUSIONS Our data show from have an unbalanced ability produce IFNγ kill target suggesting existence complex differences governed KIR-HLA interaction, particularly on KIR3DL1 expressing cells.