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Genetic relationships between A20/TNFAIP3, chronic inflammation and autoimrnune disease

Lars Vereecke UGent, Rudi Beyaert UGent and Geert van Loo UGent (2011) BIOCHEMICAL SOCIETY TRANSACTIONS. 39. p.1086-1091
abstract
A20 [also known as TNFAIP3 (tumour necrosis factor a-induced protein 3)] restricts and terminates inflammatory responses through modulation of the ubiquitination status of central components in NF-kappa B (nuclear factor kappa B), IRF3 (interferon regulatory factor 3) and apoptosis signalling cascades. The phenotype of mice with full or conditional A20 deletion illustrates that A20 expression is essential to prevent chronic inflammation and autoimmune pathology. In addition, polymorphisms within the A20 genomic locus have been associated with multiple inflammatory and autoimmune disorders, including SLE (systemic lupus erythaematosis), RA (rheumatoid arthritis), Crohn's disease and psoriasis. A20 has also been implicated as a tumour suppressor in several subsets of B-cell lymphomas. The present review outlines recent findings that illustrate the effect of A20 defects in disease pathogenesis and summarizes the identified A20 polymorphisms associated with different immunopathologies.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
GENOME-WIDE ASSOCIATION, JAPANESE POPULATION, MULTIPLE AUTOIMMUNE-DISEASES, SYSTEMIC-LUPUS-ERYTHEMATOSUS, NF-KAPPA-B, RHEUMATOID-ARTHRITIS, SUSCEPTIBILITY LOCI, A20 DEFICIENCY, CELIAC-DISEASE, CELL LYMPHOMA, A20, autoimmunity, B-cell, inflammatory bowel disease (IBD), nuclear factor kappa B (NF-kappa B), tumour necrosis factor alpha-induced protein 3 (TNFAIP3)
journal title
BIOCHEMICAL SOCIETY TRANSACTIONS
Biochem. Soc. Trans.
volume
39
pages
1086 - 1091
Web of Science type
Article
Web of Science id
000293814800043
JCR category
BIOCHEMISTRY & MOLECULAR BIOLOGY
JCR impact factor
3.711 (2011)
JCR rank
94/286 (2011)
JCR quartile
2 (2011)
ISSN
0300-5127
DOI
10.1042/BST0391086
project
Ghent researchers on unfolded proteins in inflammatory disease (GROUP-ID)
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
1892640
handle
http://hdl.handle.net/1854/LU-1892640
date created
2011-08-25 16:46:23
date last changed
2016-12-19 15:41:56
@article{1892640,
  abstract     = {A20 [also known as TNFAIP3 (tumour necrosis factor a-induced protein 3)] restricts and terminates inflammatory responses through modulation of the ubiquitination status of central components in NF-kappa B (nuclear factor kappa B), IRF3 (interferon regulatory factor 3) and apoptosis signalling cascades. The phenotype of mice with full or conditional A20 deletion illustrates that A20 expression is essential to prevent chronic inflammation and autoimmune pathology. In addition, polymorphisms within the A20 genomic locus have been associated with multiple inflammatory and autoimmune disorders, including SLE (systemic lupus erythaematosis), RA (rheumatoid arthritis), Crohn's disease and psoriasis. A20 has also been implicated as a tumour suppressor in several subsets of B-cell lymphomas. The present review outlines recent findings that illustrate the effect of A20 defects in disease pathogenesis and summarizes the identified A20 polymorphisms associated with different immunopathologies.},
  author       = {Vereecke, Lars and Beyaert, Rudi and van Loo, Geert},
  issn         = {0300-5127},
  journal      = {BIOCHEMICAL SOCIETY TRANSACTIONS},
  keyword      = {GENOME-WIDE ASSOCIATION,JAPANESE POPULATION,MULTIPLE AUTOIMMUNE-DISEASES,SYSTEMIC-LUPUS-ERYTHEMATOSUS,NF-KAPPA-B,RHEUMATOID-ARTHRITIS,SUSCEPTIBILITY LOCI,A20 DEFICIENCY,CELIAC-DISEASE,CELL LYMPHOMA,A20,autoimmunity,B-cell,inflammatory bowel disease (IBD),nuclear factor kappa B (NF-kappa B),tumour necrosis factor alpha-induced protein 3 (TNFAIP3)},
  language     = {eng},
  pages        = {1086--1091},
  title        = {Genetic relationships between A20/TNFAIP3, chronic inflammation and autoimrnune disease},
  url          = {http://dx.doi.org/10.1042/BST0391086},
  volume       = {39},
  year         = {2011},
}

Chicago
Vereecke, Lars, Rudi Beyaert, and Geert van Loo. 2011. “Genetic Relationships Between A20/TNFAIP3, Chronic Inflammation and Autoimrnune Disease.” Biochemical Society Transactions 39: 1086–1091.
APA
Vereecke, L., Beyaert, R., & van Loo, G. (2011). Genetic relationships between A20/TNFAIP3, chronic inflammation and autoimrnune disease. BIOCHEMICAL SOCIETY TRANSACTIONS, 39, 1086–1091.
Vancouver
1.
Vereecke L, Beyaert R, van Loo G. Genetic relationships between A20/TNFAIP3, chronic inflammation and autoimrnune disease. BIOCHEMICAL SOCIETY TRANSACTIONS. 2011;39:1086–91.
MLA
Vereecke, Lars, Rudi Beyaert, and Geert van Loo. “Genetic Relationships Between A20/TNFAIP3, Chronic Inflammation and Autoimrnune Disease.” BIOCHEMICAL SOCIETY TRANSACTIONS 39 (2011): 1086–1091. Print.