Common HIV-1 peptide variants mediate differential binding of KIR3DL1 to HLA-Bw4 molecules.

نویسندگان

  • Lena Fadda
  • Geraldine M O'Connor
  • Swati Kumar
  • Alicja Piechocka-Trocha
  • Clair M Gardiner
  • Mary Carrington
  • Daniel W McVicar
  • Marcus Altfeld
چکیده

Epidemiological studies have shown the protective effect of KIR3DL1/HLA-Bw4 genotypes in human immunodeficiency virus type 1 (HIV-1) infection; however, the functional correlates for the protective effect remain unknown. We investigated whether human leukocyte antigen (HLA)-Bw4-presented HIV-1 peptides could affect the interaction between the inhibitory natural killer (NK) cell receptor KIR3DL1 and its ligand HLA-Bw4. Distinct HIV-1 epitopes differentially modulated the binding of KIR3DL1 to HLA-Bw4. Furthermore, cytotoxic T lymphocyte (CTL) escape mutations within the immunodominant HLA-B57 (Bw4)-restricted Gag epitope TSTLQEQIGW abrogated KIR3DL1 binding to HLA-B57, suggesting that sensing of CTL escape variants by NK cells can contribute to the protective effect of the KIR3DL1/HLA-Bw4 compound genotype.

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عنوان ژورنال:
  • Journal of virology

دوره 85 12  شماره 

صفحات  -

تاریخ انتشار 2011