A20 Protects Against Arthritis by Regulation of the NLRP3 Inflammasome.
10.4167/jbv.2015.45.3.282
- Author:
Zahid MANZOOR
1
;
Young Sang KOH
Author Information
1. Department of Microbiology and Immunology, School of Medicine and Brain Korea 21 PLUS Program, and Institute of Medical Science, Jeju National University, Jeju, Korea. yskoh7@jejunu.ac.kr
- Publication Type:Letter
- Keywords:
A20;
Nod-like receptor pyrin domain-containing protein 3;
Inflammasome;
Rheumatoid arthritis
- MeSH:
Animals;
Arthritis*;
Arthritis, Rheumatoid;
B-Lymphocytes;
Humans;
Inflammation;
Joints;
Mice;
Necrosis
- From:Journal of Bacteriology and Virology
2015;45(3):282-284
- CountryRepublic of Korea
- Language:English
-
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-kappaB) 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.
