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Prostaglandin E2 and SOCS1 have a role in intestinal immune tolerance

Author

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  • Takatoshi Chinen

    (Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
    Graduate School of Medical Sciences, Kyushu University)

  • Kyoko Komai

    (Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
    Japan Science and Technology Agency, CREST, Chiyoda-ku, Tokyo 102-0075, Japan.)

  • Go Muto

    (Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
    Japan Science and Technology Agency, CREST, Chiyoda-ku, Tokyo 102-0075, Japan.)

  • Rimpei Morita

    (Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
    Japan Science and Technology Agency, CREST, Chiyoda-ku, Tokyo 102-0075, Japan.)

  • Naoko Inoue

    (Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
    Japan Science and Technology Agency, CREST, Chiyoda-ku, Tokyo 102-0075, Japan.)

  • Hideyuki Yoshida

    (Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
    Japan Science and Technology Agency, CREST, Chiyoda-ku, Tokyo 102-0075, Japan.)

  • Takashi Sekiya

    (Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
    Japan Science and Technology Agency, CREST, Chiyoda-ku, Tokyo 102-0075, Japan.)

  • Ryoko Yoshida

    (Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
    Japan Science and Technology Agency, CREST, Chiyoda-ku, Tokyo 102-0075, Japan.)

  • Kazuhiko Nakamura

    (Graduate School of Medical Sciences, Kyushu University)

  • Ryoichi Takayanagi

    (Graduate School of Medical Sciences, Kyushu University)

  • Akihiko Yoshimura

    (Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
    Japan Science and Technology Agency, CREST, Chiyoda-ku, Tokyo 102-0075, Japan.)

Abstract

Interleukin 10 (IL-10) and regulatory T cells (Tregs) maintain tolerance to intestinal microorganisms. However, Il10−/−Rag2−/− mice, which lack IL-10 and Tregs, remain healthy, suggesting the existence of other mechanisms of tolerance. Here, we identify suppressor of cytokine signalling 1 (SOCS1) as an essential mediator of immune tolerance in the intestine. Socs1−/−Rag2−/− mice develop severe colitis, which can be prevented by the reduction of microbiota and the transfer of IL-10-sufficient Tregs. Additionally, we find an essential role for prostaglandin E2 (PGE2) in the maintenance of tolerance within the intestine in the absence of Tregs. Socs1−/− dendritic cells are resistant to PGE2-mediated immunosuppression because of dysregulated cytokine signalling. Thus, we propose that SOCS1 and PGE2, potentially interacting together, act as an alternative intestinal tolerance mechanism distinct from IL-10 and Tregs.

Suggested Citation

  • Takatoshi Chinen & Kyoko Komai & Go Muto & Rimpei Morita & Naoko Inoue & Hideyuki Yoshida & Takashi Sekiya & Ryoko Yoshida & Kazuhiko Nakamura & Ryoichi Takayanagi & Akihiko Yoshimura, 2011. "Prostaglandin E2 and SOCS1 have a role in intestinal immune tolerance," Nature Communications, Nature, vol. 2(1), pages 1-11, September.
    • Handle: RePEc:nat:natcom:v:2:y:2011:i:1:d:10.1038_ncomms1181
    DOI: 10.1038/ncomms1181
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    Cited by:

    1. Matteo Villa & David E. Sanin & Petya Apostolova & Mauro Corrado & Agnieszka M. Kabat & Carmine Cristinzio & Annamaria Regina & Gustavo E. Carrizo & Nisha Rana & Michal A. Stanczak & Francesc Baixauli, 2024. "Prostaglandin E2 controls the metabolic adaptation of T cells to the intestinal microenvironment," Nature Communications, Nature, vol. 15(1), pages 1-19, December.

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