Open AccessContribution of Toll-Like Receptors and the NLRP3 Inflammasome in Rheumatoid Arthritis Pathophysiology
Author(s) -
S. Herbert Unterberger,
Kevin Davies,
Srinivasa Bhargav Rambhatla,
Sandra Sacre
Publication year - 2021
Publication title -
immunotargets and therapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.256
H-Index - 7
ISSN - 2253-1556
DOI - 10.2147/itt.s288547
Subject(s) - inflammasome , rheumatoid arthritis , pyrin domain , inflammation , immunology , medicine , receptor , tumor necrosis factor alpha , arthritis , innate immune system , immune system
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-1β. 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.