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A narrative review of positive regulation of NLRP3 inflammasome in rheumatoid arthritis

Journal

ANNALS OF PALLIATIVE MEDICINE
Volume 10, Issue 12, Pages 12877-12885

Publisher

AME PUBL CO
DOI: 10.21037/apm-21-3472

Keywords

Inflammasome; NOD-like receptor family pyrin domain containing 3 (NLRP3); autoimmune disease; rheumatoid arthritis (RA)

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This paper briefly reviews the features and regulatory mechanism of NLRP3 inflammasome, as well as its relationship with RA. It highlights the potential of NLRP3 inflammasome in RA treatment, enriching the therapeutic strategies for inflammatory diseases.
Objective: This paper briefly reviews the pathological characteristics and regulatory mechanism of NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome and summarizes the relationship between it and rheumatoid arthritis (RA) as a means to improve its therapeutic potential and clinical application. Background: RA is a systemic inflammatory disease with a high incidence rate. The early diagnosis and treatment of the disease is difficult, and the current treatment effect of most patients is not significant and accompanied by serious infection risk. Inflammation is an immune protective mechanism in the body. Inflammasome is an intracellular multi-body protein that stimulates the inflammatory response [inducing the release of pro-inflammatory cytokine interleukin (IL)-1 beta and IL-18] and promotes the death of thermophiles. The NLRP3 inflammatory bodies are assembled from NLRP3, apoptosis-associated speck-like protein (ASC), and pro-caspase-1. Previous studies have enriched our understanding of the activation mechanism of NLRP3 inflammasome, and animal model data suggests that it plays an important role in autoimmune diseases, including RA. Methods: Literatures about inflammation and RA were extensively reviewed to analyze and discuss. Conclusions: Especially, we focused on the role of NLRP3 inflammasome in the pathogenesis of RA and the potential of NLRP3 inflammasome or their derivatives in the treatment of RA, which enriched the treatment strategies of inflammatory diseases.

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