Progress in the relationship of A20 and NLRP3 inflammasome with juvenile idiopathic arthritis
10.3760/cma.j.cn112309-20210619-00210
- VernacularTitle:A20及NLRP3炎症小体与幼年特发性关节炎相关性研究进展
- Author:
Min PANG
1
;
Wei CAI
;
Xuemei TANG
Author Information
1. 重庆医科大学附属儿童医院风湿免疫科，儿童发育疾病研究教育部重点实验室，国家儿童健康与疾病临床医学研究中心，儿童发育重大疾病国家国际科技合作基地，儿童感染免疫重庆市重点实验室，重庆 400014
- Keywords:
A20;
NLRP3 inflammasome;
Juvenile idiopathic arthritis;
Pathogenesis;
Genetic susceptibility
- From:
Chinese Journal of Microbiology and Immunology
2022;42(2):156-160
- CountryChina
- Language:Chinese
-
Abstract:
Juvenile idiopathic arthritis (JIA) is a heterogeneous group of diseases characterized by chronic inflammatory arthritis of unknown cause, lasting six weeks or longer, and accompanied by organ damages. It is the most common chronic inflammatory rheumatic disease in childhood with unclear aetiology. A20, a protein encoded by the tumor necrosis factor α-induced protein 3 gene (TNFAIP3), regulates cell inflammatory response and apoptosis through suppressing inflammatory NF-κB signaling by acting as an ubiquitin-editing enzyme. NOD-like receptor protein 3 (NLRP3) inflammasome, a multiprotein complex formed by a subgroup of intracellular pattern recognition receptors, mediates the activation of caspase-1 and the secretion of proinflammatory cytokines IL-1β and IL-18 in response to microbial infection and cellular damage. A20 could directly reduce the basal expression of NLRP3 to impair caspase-1 activation and inhibit the assembling of NLRP3 inflammasome by suppressing the activation of NF-κB, playing a crucial anti-inflammatory role in JIA. A20 and NLRP3 inflammasome may be promising prognostic markers and therapeutic targets in JIA. This review summarized the structure and biological function of A20 and NLRP3 inflammasome and analyzed their roles in the genetic susceptibility and pathogenesis of JIA.
