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Quantity of HLA-C surface expression and licensing of KIR2DL+ natural killer cells

Charoudeh, Hojjatollah ; Schmied, Laurent ; Gonzalez, Asensio ; Terszowski, Grzegorz ; Czaja, Karol ; Schmitter, Karin ; Infanti, Laura ; Buser, Andreas ; Stern, Martin

In: Immunogenetics, 2012, vol. 64, no. 10, p. 739-745

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    Titel
    • Quantity of HLA-C surface expression and licensing of KIR2DL+ natural killer cells
    Autor
    • Charoudeh, Hojjatollah. Immunotherapy Laboratory, Department of Biomedicine, University Hospital Basel, Hebelstrasse 20, 4031, Basel, Switzerland
    • Schmied, Laurent. Immunotherapy Laboratory, Department of Biomedicine, University Hospital Basel, Hebelstrasse 20, 4031, Basel, Switzerland
    • Gonzalez, Asensio. Immunotherapy Laboratory, Department of Biomedicine, University Hospital Basel, Hebelstrasse 20, 4031, Basel, Switzerland
    • Terszowski, Grzegorz. Immunotherapy Laboratory, Department of Biomedicine, University Hospital Basel, Hebelstrasse 20, 4031, Basel, Switzerland
    • Czaja, Karol. Immunotherapy Laboratory, Department of Biomedicine, University Hospital Basel, Hebelstrasse 20, 4031, Basel, Switzerland
    • Schmitter, Karin. Immunotherapy Laboratory, Department of Biomedicine, University Hospital Basel, Hebelstrasse 20, 4031, Basel, Switzerland
    • Infanti, Laura. Blood Bank, University Hospital Basel, Basel, Switzerland
    • Buser, Andreas. Blood Bank, University Hospital Basel, Basel, Switzerland
    • Stern, Martin. Immunotherapy Laboratory, Department of Biomedicine, University Hospital Basel, Hebelstrasse 20, 4031, Basel, Switzerland
    Dokumententyp
    • Postprint
    OAI-PMH-ID
    • oai:doc.rero.ch:313221
    Summary
    Natural killer (NK) cells require interaction of inhibitory surface receptors with human leukocyte antigen (HLA) ligands during development to acquire functional competence in a process termed "licensing.” The quantity of HLA required for this process is unknown. Two polymorphisms affecting HLA-C surface expression (rs9264942 and rs67384697) have recently been identified, and shown to influence progression of HIV infection. We typed a cohort of healthy donors for the two HLA-C-related polymorphisms, KIR2DL1 and KIR2DL3, and their respective HLA-C ligands and analyzed how HLA ligands influenced licensing status of killer cell immunoglobulin-like receptor (KIR)+ NK cells in terms of degranulation and cytokine production in response to HLA-deficient target cells. The presence of respective HLA class I ligands increased the function of KIR2DL1+ and KIR2DL3+ NK cells in a dose-dependent manner. In contrast, neither of the HLA-C-related polymorphisms nor the quantity of cell surface HLA-C had any significant effect on NK cell function. Interestingly, HLA-Cw7—an HLA-C allele with low surface expression—licensed KIR2DL3+ NK cells more strongly than any other KIR2DL3 ligand. The quantity of cell surface HLA-C does not appear to influence licensing of NK cells, and the HLA-C-related polymorphisms presumably influence HIV progression through factors unrelated to NK cell education