Department for Molecular Biomedical Research, Unit of Molecular Signal Transduction in Inflammation, VIB, B-9052 Ghent, Belgium.
Biochem Soc Trans. 2011 Aug;39(4):1086-91. doi: 10.1042/BST0391086.
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.
A20（也称为 TNFAIP3，肿瘤坏死因子α诱导蛋白 3）通过调节 NF-κB（核因子 κB）、IRF3（干扰素调节因子 3）和凋亡信号级联反应中的核心成分的泛素化状态来限制和终止炎症反应。完全或条件性 A20 缺失的小鼠表型表明，A20 的表达对于防止慢性炎症和自身免疫病理学至关重要。此外，A20 基因组位点内的多态性与多种炎症和自身免疫性疾病有关，包括系统性红斑狼疮（SLE）、类风湿性关节炎（RA）、克罗恩病和银屑病。A20 也被认为是几种 B 细胞淋巴瘤的肿瘤抑制因子。本综述概述了最近的发现，这些发现说明了 A20 缺陷在疾病发病机制中的作用，并总结了与不同免疫病理学相关的已鉴定的 A20 多态性。
