Prostaglandin E2 and SOCS1 have a role in intestinal immune tolerance

Takatoshi Chinen, Kyoko Komai, Go Muto, Rimpei Morita, Naoko Inoue, Hideyuki Yoshida, Takashi Sekiya, Ryoko Yoshida, Kazuhiko Nakamura, Ryoichi Takayanagi and Akihiko Yoshimura ()
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Takatoshi Chinen: Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
Kyoko Komai: Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
Go Muto: Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
Rimpei Morita: Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
Naoko Inoue: Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
Hideyuki Yoshida: Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
Takashi Sekiya: Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
Ryoko Yoshida: Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, 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.

Nature Communications, 2011, vol. 2, issue 1, 1-11

Abstract: 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.

Date: 2011
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DOI: 10.1038/ncomms1181

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