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Molecular basis for selection and inhibition of HIV-1 escape virus by T cells and KIR2DL2+NK cells

Author

Listed:
  • Takayuki Chikata

    (Kumamoto University
    National Center for Global Health and Medicine)

  • Kimiko Kuroki

    (Hokkaido University)

  • Nozomi Kuse

    (Kumamoto University)

  • Anna E. Kliszczak

    (University of Oxford)

  • Wayne Paes

    (University of Oxford)

  • Nanami Tomioka

    (Hokkaido University)

  • Robert Parker

    (University of Oxford)

  • Aure Aflalo

    (University of Oxford)

  • Tomohiro Akahoshi

    (Kumamoto University)

  • Yu Zhang

    (Kumamoto University)

  • Ryoya Yamashita

    (Hokkaido University)

  • Ryuma Sakata

    (Hokkaido University)

  • Hiroki Kusaka

    (Hokkaido University)

  • Yosuke Watanabe

    (Hokkaido University)

  • Annalisa Nicastri

    (University of Oxford)

  • Haruki Matsubara

    (Hokkaido University)

  • Toyoyuki Ose

    (Hokkaido University)

  • Shunsuke Kita

    (Hokkaido University)

  • Shinichi Oka

    (National Center for Global Health and Medicine)

  • Hiroyuki Gatanaga

    (National Center for Global Health and Medicine)

  • Zhansong Lin

    (Kumamoto University)

  • Nicola Ternette

    (University of Oxford)

  • Persephone Borrow

    (University of Oxford)

  • Katsumi Maenaka

    (Hokkaido University
    Hokkaido University
    Hokkaido University
    Hokkaido University)

  • Masafumi Takiguchi

    (Kumamoto University)

Abstract

NK cells and CD8+ T cells both contribute to HIV-1 control. These cells not only suppress HIV-1 replication, but also select HIV-1 escape mutant viruses. Most viruses bearing T cell escape mutations are expected to remain susceptible to NK cell suppression, but their inhibition by NK cells is unclear. We investigated the role of HIV-1-specific CD8+ T cells and NK cells recognizing superimposed Pol peptides in selection and control of HIV-1 mutant virus. KIR2DL2+NK cells have an enhanced ability to recognize HIV-1-infected cells after selection of Pol mutant virus by PolIY11-specific HLA-C*12:02-restricted T cells. Mass spectrometry-based immunopeptidome profiling of HIV-1-infected cells and analysis of crystal structures of TCR- and KIR2DL2-HLA-C*12:02-peptide complexes demonstrate the molecular basis for selection and recognition of the escape mutant epitope by TCR and KIR2DL2. The present study elucidates the mechanism for selection and inhibition of an HIV-1 escape virus by T cells and NK cells.

Suggested Citation

  • Takayuki Chikata & Kimiko Kuroki & Nozomi Kuse & Anna E. Kliszczak & Wayne Paes & Nanami Tomioka & Robert Parker & Aure Aflalo & Tomohiro Akahoshi & Yu Zhang & Ryoya Yamashita & Ryuma Sakata & Hiroki , 2025. "Molecular basis for selection and inhibition of HIV-1 escape virus by T cells and KIR2DL2+NK cells," Nature Communications, Nature, vol. 16(1), pages 1-16, December.
    • Handle: RePEc:nat:natcom:v:16:y:2025:i:1:d:10.1038_s41467-025-64768-2
    DOI: 10.1038/s41467-025-64768-2
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    as
    1. Shoeib Moradi & Sanda Stankovic & Geraldine M. O’Connor & Phillip Pymm & Bruce J. MacLachlan & Camilla Faoro & Christelle Retière & Lucy C. Sullivan & Philippa M. Saunders & Jacqueline Widjaja & Shea , 2021. "Structural plasticity of KIR2DL2 and KIR2DL3 enables altered docking geometries atop HLA-C," Nature Communications, Nature, vol. 12(1), pages 1-11, December.
    2. Jeffrey C. Boyington & Shawn A. Motyka & Peter Schuck & Andrew G. Brooks & Peter D. Sun, 2000. "Crystal structure of an NK cell immunoglobulin-like receptor in complex with its class I MHC ligand," Nature, Nature, vol. 405(6786), pages 537-543, June.
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