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Paneth cells as a site of origin for intestinal inflammation

Author

Listed:
  • Timon E. Adolph

    (Addenbrooke’s Hospital, University of Cambridge, Cambridge CB2 0QQ, UK)

  • Michal F. Tomczak

    (Brigham and Women’s Hospital, Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA)

  • Lukas Niederreiter

    (Addenbrooke’s Hospital, University of Cambridge, Cambridge CB2 0QQ, UK)

  • Hyun-Jeong Ko

    (Brigham and Women’s Hospital, Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA
    Present address: Laboratory of Microbiology and Immunology, College of Pharmacy, Kangwon National University, Chuncheon 200-701, South Korea.)

  • Janne Böck

    (Institute for Clinical Molecular Biology, Christian-Albrechts-Universität zu Kiel, D-24105 Kiel, Germany)

  • Eduardo Martinez-Naves

    (Facultad de Medicina, Universidad Complutense de Madrid, 28040 Madrid, Spain)

  • Jonathan N. Glickman

    (Miraca Life Sciences)

  • Markus Tschurtschenthaler

    (Addenbrooke’s Hospital, University of Cambridge, Cambridge CB2 0QQ, UK
    Innsbruck Medical University, A-6020 Innsbruck, Austria)

  • John Hartwig

    (Brigham and Women’s Hospital, Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA)

  • Shuhei Hosomi

    (Brigham and Women’s Hospital, Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA)

  • Magdalena B. Flak

    (Brigham and Women’s Hospital, Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA)

  • Jennifer L. Cusick

    (Brigham and Women’s Hospital, Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA)

  • Kenji Kohno

    (Laboratory of Molecular and Cell Genetics, Graduate School of Biological Sciences, Nara Institute of Science and Technology (NAIST), 8916-5 Takayama, Ikoma, Nara 630-0192, Japan)

  • Takao Iwawaki

    (Advanced Scientific Research Leaders Development Unit, Gunma University 3-39-22 Showa-machi, Maebashi, Gunma 371-8511, Japan
    Iwawaki Initiative Research Unit, Advanced Science Institute, RIKEN, 2-1 Hirosawa, Wako, Saitama 351-0198, Japan)

  • Susanne Billmann-Born

    (Institute for Clinical Molecular Biology, Christian-Albrechts-Universität zu Kiel, D-24105 Kiel, Germany)

  • Tim Raine

    (Addenbrooke’s Hospital, University of Cambridge, Cambridge CB2 0QQ, UK)

  • Richa Bharti

    (Institute for Clinical Molecular Biology, Christian-Albrechts-Universität zu Kiel, D-24105 Kiel, Germany)

  • Ralph Lucius

    (Anatomical Institute, Christian-Albrechts-Universität zu Kiel, D-24098 Kiel, Germany)

  • Mi-Na Kweon

    (Mucosal Immunology Section, International Vaccine Institute)

  • Stefan J. Marciniak

    (University of Cambridge, Cambridge Institute for Medical Research (CIMR), Wellcome Trust/MRC Building, Hills Road, Cambridge CB2 0XY, UK)

  • Augustine Choi

    (Brigham and Women’s Hospital, Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA)

  • Susan J. Hagen

    (Beth Israel Deaconess Medical Center)

  • Stefan Schreiber

    (Institute for Clinical Molecular Biology, Christian-Albrechts-Universität zu Kiel, D-24105 Kiel, Germany)

  • Philip Rosenstiel

    (Institute for Clinical Molecular Biology, Christian-Albrechts-Universität zu Kiel, D-24105 Kiel, Germany)

  • Arthur Kaser

    (Addenbrooke’s Hospital, University of Cambridge, Cambridge CB2 0QQ, UK)

  • Richard S. Blumberg

    (Brigham and Women’s Hospital, Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA)

Abstract

Variation in ATG16L1, a protein involved in autophagy, confers risk for Crohn’s disease, but mice with hypomorphic ATG16L1 activity do not develop spontaneous intestinal inflammation; this study shows that autophagy compensates for endoplasmic reticulum stress — common in inflammatory bowel disease epithelium — specifically in Paneth cells, with Crohn’s-disease-like inflammation of the ileum originating from this cell type when both pathways are compromised.

Suggested Citation

  • Timon E. Adolph & Michal F. Tomczak & Lukas Niederreiter & Hyun-Jeong Ko & Janne Böck & Eduardo Martinez-Naves & Jonathan N. Glickman & Markus Tschurtschenthaler & John Hartwig & Shuhei Hosomi & Magda, 2013. "Paneth cells as a site of origin for intestinal inflammation," Nature, Nature, vol. 503(7475), pages 272-276, November.
    • Handle: RePEc:nat:nature:v:503:y:2013:i:7475:d:10.1038_nature12599
    DOI: 10.1038/nature12599
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    Citations

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    Cited by:

    1. Stéphanie Bibert & Mathieu Quinodoz & Sylvain Perriot & Fanny S. Krebs & Maxime Jan & Rita C. Malta & Emilie Collinet & Mathieu Canales & Amandine Mathias & Nicole Faignart & Eliane Roulet-Perez & Pas, 2024. "Herpes simplex encephalitis due to a mutation in an E3 ubiquitin ligase," Nature Communications, Nature, vol. 15(1), pages 1-14, December.
    2. Xingxing Ren & Qiuyuan Liu & Peirong Zhou & Tingyue Zhou & Decai Wang & Qiao Mei & Richard A. Flavell & Zhanju Liu & Mingsong Li & Wen Pan & Shu Zhu, 2024. "DHX9 maintains epithelial homeostasis by restraining R-loop-mediated genomic instability in intestinal stem cells," Nature Communications, Nature, vol. 15(1), pages 1-17, December.
    3. Ran Song & William McAlpine & Aaron M. Fond & Evan Nair-Gill & Jin Huk Choi & Elisabeth E. L. Nyström & Liisa Arike & Sydney Field & Xiaohong Li & Jeffrey A. SoRelle & James J. Moresco & Eva Marie Y. , 2023. "Trans-Golgi protein TVP23B regulates host-microbe interactions via Paneth cell homeostasis and Goblet cell glycosylation," Nature Communications, Nature, vol. 14(1), pages 1-13, December.
    4. Joachim Hanna & Flavio Beke & Louise M. O’Brien & Chrysa Kapeni & Hung-Chang Chen & Valentina Carbonaro & Alexander B. Kim & Kamal Kishore & Timon E. Adolph & Mikkel-Ole Skjoedt & Karsten Skjoedt & Ma, 2022. "Cell-autonomous Hedgehog signaling controls Th17 polarization and pathogenicity," Nature Communications, Nature, vol. 13(1), pages 1-18, December.

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