| Literature DB >> 27880898 |
Zhansong Lin1, Kimiko Kuroki2, Nozomi Kuse1, Xiaoming Sun1, Tomohiro Akahoshi1, Ying Qi3, Takayuki Chikata1, Takuya Naruto1, Madoka Koyanagi1, Hayato Murakoshi1, Hiroyuki Gatanaga4, Shinichi Oka4, Mary Carrington5, Katsumi Maenaka2, Masafumi Takiguchi6.
Abstract
Natural killer (NK) cells control viral infection in part through the interaction between killer cell immunoglobulin-like receptors (KIRs) and their human leukocyte antigen (HLA) ligands. We investigated 504 anti-retroviral (ART)-free Japanese patients chronically infected with HIV-1 and identified two KIR/HLA combinations, KIR2DL2/HLA-C∗12:02 and KIR2DL2/HLA-C∗14:03, that impact suppression of HIV-1 replication. KIR2DL2+ NK cells suppressed viral replication in HLA-C∗14:03+ or HLA-C∗12:02+ cells to a significantly greater extent than did KIR2DL2- NK cells in vitro. Functional analysis showed that the binding between HIV-1-derived peptide and HLA-C∗14:03 or HLA-C∗12:02 influenced KIR2DL2+ NK cell activity through reduced expression of the peptide-HLA (pHLA) complex on the cell surface (i.e., reduced KIR2DL2 ligand expression), rather than through reduced binding affinity of KIR2DL2 to the respective pHLA complexes. Thus, KIR2DL2/HLA-C∗12:02 and KIR2DL2/HLA-C∗14:03 compound genotypes have protective effects on control of HIV-1 through a mechanism involving KIR2DL2-mediated NK cell recognition of virus-infected cells, providing additional understanding of NK cells in HIV-1 infection. Copyright ÂEntities:
Keywords: HIV-1; HLA-C; KIR2DL2; NK cells
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Year: 2016 PMID： 27880898 PMCID： PMC5184766 DOI： 10.1016/j.celrep.2016.10.075
Source DB: PubMed Journal: Cell Rep Impact factor: 9.423