ITT-288547-contribution-of-toll-like-receptors-and-the-nlrp3-inflammaso.pdf (2.76 MB)
Contribution of toll-like receptors and the NLRP3 inflammasome in rheumatoid arthritis pathophysiology
Version 2 2023-06-12, 09:57
Version 1 2023-06-10, 00:29
journal contribution
posted on 2023-06-12, 09:57 authored by Sarah Unterberger, Kevin DaviesKevin Davies, Srinivasa Bhargav Rambhatla, Sandra SacreSandra SacreRheumatoid 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-1ß. 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.
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Publication status
- Published
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- Published version
Journal
ImmunoTargets and TherapyISSN
2253-1556Publisher
Dove Medical PressExternal DOI
Volume
10Page range
285-298Department affiliated with
- Clinical and Experimental Medicine Publications
Full text available
- Yes
Peer reviewed?
- Yes
Legacy Posted Date
2021-07-29First Open Access (FOA) Date
2021-07-29First Compliant Deposit (FCD) Date
2021-07-29Usage metrics
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