A20 [also known as TNFAIP3 (tumour necrosis factor α-induced protein 3)] restricts and terminates inflammatory responses through modulation of the ubiquitination status of central components in NF-κB (nuclear factor κB), 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.
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August 2011
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Conference Article|
July 20 2011
Genetic relationships between A20/TNFAIP3, chronic inflammation and autoimmune disease
Lars Vereecke;
Lars Vereecke
1Department for Molecular Biomedical Research, Unit of Molecular Signal Transduction in Inflammation, VIB, B-9052 Ghent, Belgium, and Department of Biomedical Molecular Biology, Ghent University, B-9052 Ghent, Belgium
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Rudi Beyaert;
Rudi Beyaert
1
1Department for Molecular Biomedical Research, Unit of Molecular Signal Transduction in Inflammation, VIB, B-9052 Ghent, Belgium, and Department of Biomedical Molecular Biology, Ghent University, B-9052 Ghent, Belgium
1Correspondence may be addressed to either of these authors (email rudi.beyaert@dmbr.vib-UGent.be or geert.vanloo@dmbr.vib-UGent.be).
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Geert van Loo
Geert van Loo
1
1Department for Molecular Biomedical Research, Unit of Molecular Signal Transduction in Inflammation, VIB, B-9052 Ghent, Belgium, and Department of Biomedical Molecular Biology, Ghent University, B-9052 Ghent, Belgium
1Correspondence may be addressed to either of these authors (email rudi.beyaert@dmbr.vib-UGent.be or geert.vanloo@dmbr.vib-UGent.be).
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Publisher: Portland Press Ltd
Received:
March 03 2011
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© The Authors Journal compilation © 2011 Biochemical Society
2011
Biochem Soc Trans (2011) 39 (4): 1086–1091.
Article history
Received:
March 03 2011
Citation
Lars Vereecke, Rudi Beyaert, Geert van Loo; Genetic relationships between A20/TNFAIP3, chronic inflammation and autoimmune disease. Biochem Soc Trans 1 August 2011; 39 (4): 1086–1091. doi: https://doi.org/10.1042/BST0391086
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