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Enterocyte-specific A20 deficiency sensitizes to tumor necrosis factor-induced toxicity and experimental colitis

Lars Vereecke UGent, Mozes Sze UGent, Conor Mc Guire UGent, Brecht Rogiers UGent, Yuanyuan Chu, Marc Schmidt-Supprian, Manolis Pasparakis, Rudi Beyaert UGent and Geert van Loo UGent (2010) JOURNAL OF EXPERIMENTAL MEDICINE. 207(7). p.1513-1523
abstract
A20 is a nuclear factor kappa B (NF-kappa B) target gene that encodes a ubiquitin-editing enzyme that is essential for the termination of NF-kappa B activation after tumor necrosis factor (TNF) or microbial product stimulation and for the prevention of TNF-induced apoptosis. Mice lacking A20 succumb to inflammation in several organs, including the intestine, and A20 mutations have been associated with Crohn's disease. However, ablation of NF-kappa B activity, specifically in intestinal epithelial cells (IECs), promotes intestinal inflammation. As A20 deficiency sensitizes cells to TNF-induced apoptosis yet also promotes NF-kappa B activity, it is not clear if A20 deficiency in IECs would exacerbate or ameliorate intestinal inflammation. We generated mice lacking A20 specifically in IECs. These mice did not show spontaneous intestinal inflammation but exhibited increased susceptibility to experimental colitis, and their IECs were hypersensitive to TNF-induced apoptosis. The resulting TNF-driven breakdown of the intestinal barrier permitted commensal bacterial infiltration and led to systemic inflammation. These studies define A20 as a major antiapoptotic protein in the intestinal epithelium and further indicate that defects in A20 might contribute to inflammatory bowel disease in humans.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
IMMUNE HOMEOSTASIS, CROHNS-DISEASE, ENZYME A20, TOLL-LIKE RECEPTORS, INFLAMMATORY-BOWEL-DISEASE, NF-KAPPA-B, MICE, GUT, RESPONSES, CELLS
journal title
JOURNAL OF EXPERIMENTAL MEDICINE
J. Exp. Med.
volume
207
issue
7
pages
1513 - 1523
Web of Science type
Article
Web of Science id
000279464700015
JCR category
MEDICINE, RESEARCH & EXPERIMENTAL
JCR impact factor
14.776 (2010)
JCR rank
2/105 (2010)
JCR quartile
1 (2010)
ISSN
0022-1007
DOI
10.1084/jem.20092474
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
1017066
handle
http://hdl.handle.net/1854/LU-1017066
date created
2010-08-03 11:17:18
date last changed
2016-12-19 15:46:23
@article{1017066,
  abstract     = {A20 is a nuclear factor kappa B (NF-kappa B) target gene that encodes a ubiquitin-editing enzyme that is essential for the termination of NF-kappa B activation after tumor necrosis factor (TNF) or microbial product stimulation and for the prevention of TNF-induced apoptosis. Mice lacking A20 succumb to inflammation in several organs, including the intestine, and A20 mutations have been associated with Crohn's disease. However, ablation of NF-kappa B activity, specifically in intestinal epithelial cells (IECs), promotes intestinal inflammation. As A20 deficiency sensitizes cells to TNF-induced apoptosis yet also promotes NF-kappa B activity, it is not clear if A20 deficiency in IECs would exacerbate or ameliorate intestinal inflammation. We generated mice lacking A20 specifically in IECs. These mice did not show spontaneous intestinal inflammation but exhibited increased susceptibility to experimental colitis, and their IECs were hypersensitive to TNF-induced apoptosis. The resulting TNF-driven breakdown of the intestinal barrier permitted commensal bacterial infiltration and led to systemic inflammation. These studies define A20 as a major antiapoptotic protein in the intestinal epithelium and further indicate that defects in A20 might contribute to inflammatory bowel disease in humans.},
  author       = {Vereecke, Lars and Sze, Mozes and Mc Guire, Conor and Rogiers, Brecht and Chu, Yuanyuan and Schmidt-Supprian, Marc and Pasparakis, Manolis and Beyaert, Rudi and van Loo, Geert},
  issn         = {0022-1007},
  journal      = {JOURNAL OF EXPERIMENTAL MEDICINE},
  keyword      = {IMMUNE HOMEOSTASIS,CROHNS-DISEASE,ENZYME A20,TOLL-LIKE RECEPTORS,INFLAMMATORY-BOWEL-DISEASE,NF-KAPPA-B,MICE,GUT,RESPONSES,CELLS},
  language     = {eng},
  number       = {7},
  pages        = {1513--1523},
  title        = {Enterocyte-specific A20 deficiency sensitizes to tumor necrosis factor-induced toxicity and experimental colitis},
  url          = {http://dx.doi.org/10.1084/jem.20092474},
  volume       = {207},
  year         = {2010},
}

Chicago
Vereecke, Lars, Mozes Sze, Conor Mc Guire, Brecht Rogiers, Yuanyuan Chu, Marc Schmidt-Supprian, Manolis Pasparakis, Rudi Beyaert, and Geert van Loo. 2010. “Enterocyte-specific A20 Deficiency Sensitizes to Tumor Necrosis Factor-induced Toxicity and Experimental Colitis.” Journal of Experimental Medicine 207 (7): 1513–1523.
APA
Vereecke, L., Sze, M., Mc Guire, C., Rogiers, B., Chu, Y., Schmidt-Supprian, M., Pasparakis, M., et al. (2010). Enterocyte-specific A20 deficiency sensitizes to tumor necrosis factor-induced toxicity and experimental colitis. JOURNAL OF EXPERIMENTAL MEDICINE, 207(7), 1513–1523.
Vancouver
1.
Vereecke L, Sze M, Mc Guire C, Rogiers B, Chu Y, Schmidt-Supprian M, et al. Enterocyte-specific A20 deficiency sensitizes to tumor necrosis factor-induced toxicity and experimental colitis. JOURNAL OF EXPERIMENTAL MEDICINE. 2010;207(7):1513–23.
MLA
Vereecke, Lars, Mozes Sze, Conor Mc Guire, et al. “Enterocyte-specific A20 Deficiency Sensitizes to Tumor Necrosis Factor-induced Toxicity and Experimental Colitis.” JOURNAL OF EXPERIMENTAL MEDICINE 207.7 (2010): 1513–1523. Print.