Abstract
Rheumatoid arthritis is an autoinflammatory disease that primarily affects joints and is characterized by pervasive joint inflammation. A20/Tumor necrosis factor, alpha-induced protein 3 (Tnfaip3) inhibits activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and has been associated with rheumatoid arthritis. However, the precise role of A20 in rheumatoid arthritis remains unclear. Deletion of A20/Tnfaip3 gene in mice elicits impulsive erosive polyarthritis that is similar to rheumatoid arthritis in patients. Recently, it has been shown that A20 protects against arthritis by regulating the NLRP3 inflammasome.
REFERENCES
1). Vande Walle L, Van Opdenbosch N, Jacques P, Fossoul A, Verheugen E, Vogel P, et al. Negative regulation of the NLRP3 inflammasome by A20 protects against arthritis. Nature. 2014; 512:69–73.
2). Manzoor Z, Koo JE, Koh YS. Mitogen-activated Protein Kinases Signaling in Inflammation-related Carcinogenesis. J Bacteriol Virol. 2014; 44:297–304.
3). Manzoor Z, Koh YS. Mitogen-activated Protein Kinases in Inflammation. J Bacteriol Virol. 2012; 42:189–95.
4). Martinon F, Burns K, Tschopp J. The inflammasome: a molecular platform triggering activation of inflammatory caspases and processing of proIL-beta. Mol Cell. 2002; 10:417–26.
5). Boone DL, Turer EE, Lee EG, Ahmad RC, Wheeler MT, Tsui C, et al. The ubiquitin-modifying enzyme A20 is required for termination of Toll-like receptor responses. Nat Immunol. 2004; 5:1052–60.