Paneth cells as a site of origin for intestinal inflammation

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, Magdalena B. Flak, Jennifer L. Cusick, Kenji Kohno, Takao Iwawaki, Susanne Billmann-Born, Tim Raine, Richa Bharti, Ralph Lucius, Mi-Na Kweon, Stefan J. Marciniak, Augustine Choi, Susan J. Hagen, Stefan Schreiber, Philip Rosenstiel, Arthur Kaser () and Richard S. Blumberg ()
Additional contact information
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
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
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
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

Nature, 2013, vol. 503, issue 7475, 272-276

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.

Date: 2013
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DOI: 10.1038/nature12599

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