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
关键词
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学科分类号
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
收藏
页码:272 / 276
页数:4
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