The role of Toll-like receptors in rheumatoid arthritis

Richard M. Pope; Qi Quan Huang

doi:10.1007/s11926-009-0051-z

The role of Toll-like receptors in rheumatoid arthritis

Richard M. Pope, Qi Quan Huang

Medicine, Rheumatology Division

Research output: Contribution to journal › Review article › peer-review

220 Scopus citations

Abstract

An increasing body of data supports the role of the innate immune system in the pathogenesis of rheumatoid arthritis (RA). Toll-like receptors (TLRs) are expressed by cells within the RA joint and various endogenous TLR ligands are present within the inflamed joints of patients with RA. Further, various animal models suggest that TLR signaling is important in the pathogenesis of disease. Overall, the data suggest that activation by endogenous TLR ligands may contribute to the persistent expression of proinflammatory cytokines by macrophages and the joint damage to cartilage and bone that occurs in RA. The data support a potential role for suppression of TLR signaling as a novel therapeutic approach in patients with RA.

Original language	English (US)
Pages (from-to)	357-364
Number of pages	8
Journal	Current rheumatology reports
Volume	11
Issue number	5
DOIs	https://doi.org/10.1007/s11926-009-0051-z
State	Published - Oct 2009

Funding

This work was supported by National Institutes of Health grant AR055240 and a Within Our Reach Grant from the American College of Rheumatology.

ASJC Scopus subject areas

Rheumatology

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10.1007/s11926-009-0051-z

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title = "The role of Toll-like receptors in rheumatoid arthritis",

abstract = "An increasing body of data supports the role of the innate immune system in the pathogenesis of rheumatoid arthritis (RA). Toll-like receptors (TLRs) are expressed by cells within the RA joint and various endogenous TLR ligands are present within the inflamed joints of patients with RA. Further, various animal models suggest that TLR signaling is important in the pathogenesis of disease. Overall, the data suggest that activation by endogenous TLR ligands may contribute to the persistent expression of proinflammatory cytokines by macrophages and the joint damage to cartilage and bone that occurs in RA. The data support a potential role for suppression of TLR signaling as a novel therapeutic approach in patients with RA.",

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N2 - An increasing body of data supports the role of the innate immune system in the pathogenesis of rheumatoid arthritis (RA). Toll-like receptors (TLRs) are expressed by cells within the RA joint and various endogenous TLR ligands are present within the inflamed joints of patients with RA. Further, various animal models suggest that TLR signaling is important in the pathogenesis of disease. Overall, the data suggest that activation by endogenous TLR ligands may contribute to the persistent expression of proinflammatory cytokines by macrophages and the joint damage to cartilage and bone that occurs in RA. The data support a potential role for suppression of TLR signaling as a novel therapeutic approach in patients with RA.

AB - An increasing body of data supports the role of the innate immune system in the pathogenesis of rheumatoid arthritis (RA). Toll-like receptors (TLRs) are expressed by cells within the RA joint and various endogenous TLR ligands are present within the inflamed joints of patients with RA. Further, various animal models suggest that TLR signaling is important in the pathogenesis of disease. Overall, the data suggest that activation by endogenous TLR ligands may contribute to the persistent expression of proinflammatory cytokines by macrophages and the joint damage to cartilage and bone that occurs in RA. The data support a potential role for suppression of TLR signaling as a novel therapeutic approach in patients with RA.

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The role of Toll-like receptors in rheumatoid arthritis

Abstract

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