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T-cell activation by transitory neo-antigens derived from distinct microbial pathways

Author

Listed:
  • Alexandra J. Corbett

    (Peter Doherty Institute for Infection and Immunity, University of Melbourne)

  • Sidonia B. G. Eckle

    (Peter Doherty Institute for Infection and Immunity, University of Melbourne)

  • Richard W. Birkinshaw

    (School of Biomedical Sciences, Monash University)

  • Ligong Liu

    (Institute for Molecular Bioscience, The University of Queensland)

  • Onisha Patel

    (School of Biomedical Sciences, Monash University)

  • Jennifer Mahony

    (School of Microbiology, University College Cork)

  • Zhenjun Chen

    (Peter Doherty Institute for Infection and Immunity, University of Melbourne)

  • Rangsima Reantragoon

    (Peter Doherty Institute for Infection and Immunity, University of Melbourne)

  • Bronwyn Meehan

    (Peter Doherty Institute for Infection and Immunity, University of Melbourne)

  • Hanwei Cao

    (Peter Doherty Institute for Infection and Immunity, University of Melbourne)

  • Nicholas A. Williamson

    (The Bio21 Molecular Science and Biotechnology Institute, University of Melbourne)

  • Richard A. Strugnell

    (Peter Doherty Institute for Infection and Immunity, University of Melbourne)

  • Douwe Van Sinderen

    (School of Microbiology, University College Cork
    Alimentary Pharmabiotic Centre, University College Cork)

  • Jeffrey Y. W. Mak

    (Institute for Molecular Bioscience, The University of Queensland)

  • David P. Fairlie

    (Institute for Molecular Bioscience, The University of Queensland
    Australian Research Council Centre of Excellence in Advanced Molecular Imaging, The University of Queensland)

  • Lars Kjer-Nielsen

    (Peter Doherty Institute for Infection and Immunity, University of Melbourne)

  • Jamie Rossjohn

    (School of Biomedical Sciences, Monash University
    Australian Research Council Centre of Excellence in Advanced Molecular Imaging, Monash University
    Institute of Infection and Immunity, Cardiff University, School of Medicine, Heath Park, Cardiff CF14 4XN, UK)

  • James McCluskey

    (Peter Doherty Institute for Infection and Immunity, University of Melbourne)

Abstract

Activation of mucosal-associated invariant T (MAIT) cells is shown to require key genes encoding an early intermediate in bacterial riboflavin synthesis, 5-amino-6-d-ribitylaminouracil; this reacts non-enzymatically with metabolites to form short-lived antigens that are captured and stabilized by MR1 for presentation to MAIT cells.

Suggested Citation

  • Alexandra J. Corbett & Sidonia B. G. Eckle & Richard W. Birkinshaw & Ligong Liu & Onisha Patel & Jennifer Mahony & Zhenjun Chen & Rangsima Reantragoon & Bronwyn Meehan & Hanwei Cao & Nicholas A. Willi, 2014. "T-cell activation by transitory neo-antigens derived from distinct microbial pathways," Nature, Nature, vol. 509(7500), pages 361-365, May.
  • Handle: RePEc:nat:nature:v:509:y:2014:i:7500:d:10.1038_nature13160
    DOI: 10.1038/nature13160
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    Cited by:

    1. Mark Walkenhorst & Jana K. Sonner & Nina Meurs & Jan Broder Engler & Simone Bauer & Ingo Winschel & Marcel S. Woo & Lukas Raich & Iris Winkler & Vanessa Vieira & Lisa Unger & Gabriela Salinas & Olivie, 2024. "Protective effect of TCR-mediated MAIT cell activation during experimental autoimmune encephalomyelitis," Nature Communications, Nature, vol. 15(1), pages 1-16, December.
    2. Ann-Christin Gnirck & Marie-Sophie Philipp & Alex Waterhölter & Malte Wunderlich & Nikhat Shaikh & Virginia Adamiak & Lena Henneken & Tobias Kautz & Tingting Xiong & Daniela Klaus & Pascal Tomczyk & M, 2023. "Mucosal-associated invariant T cells contribute to suppression of inflammatory myeloid cells in immune-mediated kidney disease," Nature Communications, Nature, vol. 14(1), pages 1-16, December.
    3. Kensuke Shibata & Chihiro Motozono & Masamichi Nagae & Takashi Shimizu & Eri Ishikawa & Daisuke Motooka & Daisuke Okuzaki & Yoshihiro Izumi & Masatomo Takahashi & Nao Fujimori & James B. Wing & Takahi, 2022. "Symbiotic bacteria-dependent expansion of MR1-reactive T cells causes autoimmunity in the absence of Bcl11b," Nature Communications, Nature, vol. 13(1), pages 1-15, December.

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