Paneth cells as a site of origin for intestinal inflammation

被引：0

作者：

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

Richard S. Blumberg

机构：

[1] Addenbrooke’s Hospital,Division of Gastroenterology and Hepatology, Department of Medicine

[2] University of Cambridge,Division of Gastroenterology, Department of Medicine

[3] Cambridge CB2 0QQ,Department of Microbiology and Immunology

[4] UK,GI Pathology Division

[5] Brigham and Women’s Hospital,Department of Medicine

[6] Harvard Medical School,Translational Medicine Division, Department of Medicine

[7] 75 Francis Street,Laboratory Science Division

[8] Boston,Department of Medicine

[9] Massachusetts 02115,Division of Pulmonary and Critical Care Medicine, Department of Medicine

[10] USA,Department of Surgery

[11] Institute for Clinical Molecular Biology,undefined

[12] Christian-Albrechts-Universität zu Kiel,undefined

[13] D-24105 Kiel,undefined

[14] Germany,undefined

[15] Facultad de Medicina,undefined

[16] Universidad Complutense de Madrid,undefined

[17] 28040 Madrid,undefined

[18] Spain,undefined

[19] Miraca Life Sciences,undefined

[20] Innsbruck Medical University,undefined

[21] A-6020 Innsbruck,undefined

[22] Austria,undefined

[23] Brigham and Women’s Hospital,undefined

[24] Harvard Medical School,undefined

[25] 75 Francis Street,undefined

[26] Boston,undefined

[27] Massachusetts 02115,undefined

[28] USA,undefined

[29] Laboratory of Molecular and Cell Genetics,undefined

[30] Graduate School of Biological Sciences,undefined

[31] Nara Institute of Science and Technology (NAIST),undefined

[32] 8916-5 Takayama,undefined

[33] Ikoma,undefined

[34] Nara 630-0192,undefined

[35] Japan,undefined

[36] Advanced Scientific Research Leaders Development Unit,undefined

[37] Gunma University 3-39-22 Showa-machi,undefined

[38] Maebashi,undefined

[39] Gunma 371-8511,undefined

[40] Japan,undefined

[41] Iwawaki Initiative Research Unit,undefined

[42] Advanced Science Institute,undefined

[43] RIKEN,undefined

[44] 2-1 Hirosawa,undefined

[45] Wako,undefined

[46] Saitama 351-0198,undefined

[47] Japan,undefined

[48] Anatomical Institute,undefined

[49] Christian-Albrechts-Universität zu Kiel,undefined

[50] D-24098 Kiel,undefined

来源：

Nature | 2013年 / 503卷

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摘要：

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.

引用

页码：272 / 276

页数：4

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