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Nucleic acid sensing by T cells initiates Th2 cell differentiation

Author

Listed:
  • Takayuki Imanishi

    (Laboratory for Cell Signaling, RCAI, RIKEN Center for Integrative Medical Sciences (IMS-RCAI))

  • Chitose Ishihara

    (Laboratory for Cell Signaling, RCAI, RIKEN Center for Integrative Medical Sciences (IMS-RCAI))

  • Mohamed El Sherif Gadelhaq Badr

    (Laboratory for Cell Signaling, RCAI, RIKEN Center for Integrative Medical Sciences (IMS-RCAI))

  • Akiko Hashimoto-Tane

    (Laboratory for Cell Signaling, RCAI, RIKEN Center for Integrative Medical Sciences (IMS-RCAI))

  • Yayoi Kimura

    (Graduate School of Medical Life Sciences, Yokohama City University)

  • Taro Kawai

    (Laboratory of Host Defense, WPI Immunology Frontier Research Center, Osaka University
    Present address: Laboratory of Molecular Immunobiology, Graduate School of Biological Sciences, Nara Institute of Science and Technology (NAIST), Ikoma, Nara 630-0192, Japan)

  • Osamu Takeuchi

    (Laboratory of Host Defense, WPI Immunology Frontier Research Center, Osaka University
    Present address: Laboratory of Infection and Prevention, Institute for Virus Research, Kyoto University, Sakyo-ku, Kyoto 606-8507, Japan)

  • Ken J. Ishii

    (Laboratory of Adjuvant Innovation, National Institute of Biomedical Innovation
    Laboratories of Vaccine Science, WPI Immunology Frontier Research, Osaka University)

  • Shun'ichiro Taniguchi

    (Institute of Pathogenesis and Disease Prevention, Shinshu University Graduate School of Medicine)

  • Tetsuo Noda

    (Cancer Research Institute of the Japanese Foundation of Cancer Research)

  • Hisashi Hirano

    (Graduate School of Medical Life Sciences, Yokohama City University)

  • Frank Brombacher

    (International Center for Genetic Engineering and Biotechnology, Cape Town Component and Institute of Infectious Diseases and Molecular Medicine, Faculty of Health Science, University of Cape Town)

  • Glen N. Barber

    (University of Miami Miller School of Medicine)

  • Shizuo Akira

    (Laboratory of Host Defense, WPI Immunology Frontier Research Center, Osaka University)

  • Takashi Saito

    (Laboratory for Cell Signaling, RCAI, RIKEN Center for Integrative Medical Sciences (IMS-RCAI)
    Laboratory for Cell Signaling, WPI Immunology Frontier Research Center, Osaka University)

Abstract

While T-cell responses are directly modulated by Toll-like receptor (TLR) ligands, the mechanism and physiological function of nucleic acids (NAs)-mediated T cell costimulation remains unclear. Here we show that unlike in innate cells, T-cell costimulation is induced even by non-CpG DNA and by self-DNA, which is released from dead cells and complexes with antimicrobial peptides or histones. Such NA complexes are internalized by T cells and induce costimulatory responses independently of known NA sensors, including TLRs, RIG-I-like receptors (RLRs), inflammasomes and STING-dependent cytosolic DNA sensors. Such NA-mediated costimulation crucially induces Th2 differentiation by suppressing T-bet expression, followed by the induction of GATA-3 and Th2 cytokines. These findings unveil the function of NA sensing by T cells to trigger and amplify allergic inflammation.

Suggested Citation

  • Takayuki Imanishi & Chitose Ishihara & Mohamed El Sherif Gadelhaq Badr & Akiko Hashimoto-Tane & Yayoi Kimura & Taro Kawai & Osamu Takeuchi & Ken J. Ishii & Shun'ichiro Taniguchi & Tetsuo Noda & Hisash, 2014. "Nucleic acid sensing by T cells initiates Th2 cell differentiation," Nature Communications, Nature, vol. 5(1), pages 1-12, May.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms4566
    DOI: 10.1038/ncomms4566
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