@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},
  keywords     = {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},
}

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