A20: a master regulator of arthritis
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REVIEW
Open Access
A20: a master regulator of arthritis Yongyao Wu1†, Xiaomin He1†, Ning Huang1†, Jiayun Yu2 and Bin Shao1,2*
Abstract A20, also known as TNF-α-induced protein 3 (TNFAIP3), is an anti-inflammatory protein that plays an important part in both immune responses and cell death. Impaired A20 function is associated with several human inflammatory and autoimmune diseases. Although the role of A20 in mediating inflammation has been frequently discussed, its intrinsic link to arthritis awaits further explanation. Here, we review new findings that further demonstrate the molecular mechanisms through which A20 regulates inflammatory arthritis, and we discuss the regulation of A20 by many factors. We conclude by reviewing the latest A20-associated mouse models that have been applied in related research because they reflect the characteristics of arthritis, the study of which will hopefully cast new light on anti-arthritis treatments. Keywords: A20, Arthritis, Zinc finger domains, Inflammation, Mouse models
Introduction Arthritis has long attracted much attention due to its multifaceted influence on human health; the three most common types are rheumatoid arthritis (RA), osteoarthritis (OA), and spondyloarthritis (SpA) [1]. RA, characterized by painful swollen joints and progressive bone erosion, is an autoimmune disease that severely impairs physical function and quality of life [2]. OA is the primary cause of disability and source of societal expenditure in elderly adults, which has become even more prevalent recently than it has been in preceding decades [3]. What is worse, there have been non-significant differences to patients’ mortality risk and functional disability between a decade ago and now, but patients’ expectations of efficient treatment have increased [4]. Therefore, it is meaningful to explore innovative therapeutic strategies for arthritis. RA, OA, and SpA can be distinguished based on their diversity in pathogenesis and manifestations, but they * Correspondence: [email protected] † Yongyao Wu, Xiaomin He and Ning Huang contributed equally to this work. 1 State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China 2 State Key Laboratory of Biotherapy anf Cancer Center, West China Hospital, Sichuan University, Chengdu 610041, China
demonstrate analogous inflammatory features; however, not all signs of inflammation appear in joints [1]. In addition, many inflammation-related pathways, such as the tumor necrosis factor receptor (TNFR)-induced nuclear factor kappa B (NF-κB) pathway, mitogen-activated protein kinase (MAPK) signaling, and Janus kinasesignal transducer and activator of transcription (JAKSTAT) signaling, are highly associated with these diseases [5–7]. Pro-inflammatory family members, which can be detected in the articular environment when arthritis occurs, are associated with the degree of inflammation present [8]. On the one hand, some proinflammatory cytokines, such
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