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Helminth-induced IL-4 expands bystander memory CD8+ T cells for early control of viral infection

Author

Listed:
  • Marion Rolot

    (University of Liège)

  • Annette M. Dougall

    (University of Liège)

  • Alisha Chetty

    (University of Cape Town)

  • Justine Javaux

    (University of Liège)

  • Ting Chen

    (University of Liège)

  • Xue Xiao

    (University of Liège)

  • Bénédicte Machiels

    (University of Liège)

  • Murray E. Selkirk

    (Imperial College London)

  • Rick M. Maizels

    (University of Glasgow)

  • Cornelis Hokke

    (Leiden University Medical Center)

  • Olivier Denis

    (Communicable and Infectious Diseases)

  • Frank Brombacher

    (University of Cape Town
    International Centre for Genetic Engineering and Biotechnology
    South African Medical Research Council (SAMRC))

  • Alain Vanderplasschen

    (University of Liège)

  • Laurent Gillet

    (University of Liège)

  • William G. C. Horsnell

    (University of Cape Town
    University of Birmingham
    CNRS-University of Orleans and Le Studium Institute for Advanced Studies, Rue Dupanloup)

  • Benjamin G. Dewals

    (University of Liège)

Abstract

Infection with parasitic helminths can imprint the immune system to modulate bystander inflammatory processes. Bystander or virtual memory CD8+ T cells (TVM) are non-conventional T cells displaying memory properties that can be generated through responsiveness to interleukin (IL)-4. However, it is not clear if helminth-induced type 2 immunity functionally affects the TVM compartment. Here, we show that helminths expand CD44hiCD62LhiCXCR3hiCD49dlo TVM cells through direct IL-4 signaling in CD8+ T cells. Importantly, helminth-mediated conditioning of TVM cells provided enhanced control of acute respiratory infection with the murid gammaherpesvirus 4 (MuHV-4). This enhanced control of MuHV-4 infection could further be explained by an increase in antigen-specific CD8+ T cell effector responses in the lung and was directly dependent on IL-4 signaling. These results demonstrate that IL-4 during helminth infection can non-specifically condition CD8+ T cells, leading to a subsequently raised antigen-specific CD8+ T cell activation that enhances control of viral infection.

Suggested Citation

  • Marion Rolot & Annette M. Dougall & Alisha Chetty & Justine Javaux & Ting Chen & Xue Xiao & Bénédicte Machiels & Murray E. Selkirk & Rick M. Maizels & Cornelis Hokke & Olivier Denis & Frank Brombacher, 2018. "Helminth-induced IL-4 expands bystander memory CD8+ T cells for early control of viral infection," Nature Communications, Nature, vol. 9(1), pages 1-16, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-06978-5
    DOI: 10.1038/s41467-018-06978-5
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    Cited by:

    1. Sonwabile Dzanibe & Aaron J. Wilk & Susan Canny & Thanmayi Ranganath & Berenice Alinde & Florian Rubelt & Huang Huang & Mark M. Davis & Susan P. Holmes & Heather B. Jaspan & Catherine A. Blish & Clive, 2024. "Premature skewing of T cell receptor clonality and delayed memory expansion in HIV-exposed infants," Nature Communications, Nature, vol. 15(1), pages 1-15, December.
    2. Ruining Liu & Victoria Muliadi & Wenjun Mou & Hanxiong Li & Juan Yuan & Johan Holmberg & Benedict J. Chambers & Nadeem Ullah & Jakob Wurth & Mohammad Alzrigat & Susanne Schlisio & Berit Carow & Lars G, 2022. "HIF-1 stabilization in T cells hampers the control of Mycobacterium tuberculosis infection," Nature Communications, Nature, vol. 13(1), pages 1-20, December.

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