Nucleic acid sensing by T cells initiates Th2 cell differentiation

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, Hisashi Hirano, Frank Brombacher, Glen N. Barber, Shizuo Akira and Takashi Saito ()
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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
Osamu Takeuchi: Laboratory of Host Defense, WPI Immunology Frontier Research Center, Osaka University
Ken J. Ishii: Laboratory of Adjuvant Innovation, National Institute of Biomedical Innovation
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)

Nature Communications, 2014, vol. 5, issue 1, 1-12

Abstract: 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.

Date: 2014
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DOI: 10.1038/ncomms4566

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