Contribution of Toll-Like Receptors and the NLRP3 Inflammasome in Rheumatoid Arthritis Pathophysiology

• Published in: ImmunoTargets and therapy Vol. 10; pp. 285 - 298
• Main Authors: Unterberger, Sarah, Davies, Kevin A, Rambhatla, Srinivasa Bhargav, Sacre, Sandra
• Format: Journal Article
• Language: English
• Published: Macclesfield Dove Medical Press Limited 01-01-2021; Taylor & Francis Ltd; Dove; Dove Medical Press
• Subjects: Antibodies; Apoptosis; Arthritis; Autoimmune diseases; Cartilage; Cytokines; Fibroblasts; il-1; IL-1β; il-6; Inflammasomes; Inflammation; Interleukin 1; Interleukin 6; Interleukins; Joint diseases; Kinases; Ligands; nlrp3 inflammasome; Proteins; Pyrin protein; Review; Rheumatoid arthritis; Rheumatoid factor; tnf; toll-like receptor; Toll-like receptors; Tumor necrosis factor; Tumor necrosis factor-TNF; Canada
• ISSN: 2253-1556; 2253-1556
• DOI: 10.2147/ITT.S288547

Rheumatoid arthritis (RA) is a progressive autoimmune disease that is characterized by inflammation of the synovial joints leading to cartilage and bone damage. The pathogenesis is sustained by the production of pro-inflammatory cytokines including tumor necrosis factor (TNF), interleukin (IL)-1 and IL-6, which can be targeted therapeutically to alleviate disease severity. Several innate immune receptors are suggested to contribute to the chronic inflammation in RA, through the production of pro-inflammatory factors in response to endogenous danger signals. Much research has focused on toll-like receptors and more recently the nucleotide-binding domain and leucine-rich repeat pyrin containing protein-3 (NLRP3) inflammasome, which is required for the processing and release of IL-1[beta]. This review summarizes the current understanding of the potential involvement of these receptors in the initiation and maintenance of inflammation and tissue damage in RA and experimental arthritis models. Keywords: rheumatoid arthritis, IL-1, IL-6, TNF, toll-like receptor, NLRP3 inflammasome