Abstract
Synovial tissue of patients with rheumatoid arthritis (RA) spontaneously produces several cytokines, of which a fundamental role in joint inflammation and destruction has been established. However, the factors sustaining this phenomenon remain poorly understood. In a recent report, blockade of Toll-like receptor 2 (TLR2) was found to inhibit the spontaneous release of inflammatory cytokines by intact RA synovial explant cultures. Adding to the recent evidence implicating other TLRs (in particular, TLR4), this observation highlights the potential of TLRs as therapeutic targets to suppress the local production of multiple cytokines and to control the chronic inflammatory loop in RA.
Highlights
Synovial tissue of patients with rheumatoid arthritis (RA) spontaneously produces several cytokines, of which a fundamental role in joint inflammation and destruction has been established
In the previous issue of Arthritis Research & Therapy, Nic An Ultaigh and colleagues [1] reported that Toll-like receptor 2 (TLR2) mediates spontaneous cytokine release from RA ex vivo synovial explant cultures
Some TLRs such as TLR2, TLR3, and TLR4 can be activated by endogenous ‘danger’ molecules associated with inflammation and tissue destruction, and many of these molecules have been found in joints and serum of patients with RA and show a positive correlation with disease activity scores [4,5]
Summary
Synovial tissue of patients with rheumatoid arthritis (RA) spontaneously produces several cytokines, of which a fundamental role in joint inflammation and destruction has been established. In the previous issue of Arthritis Research & Therapy, Nic An Ultaigh and colleagues [1] reported that Toll-like receptor 2 (TLR2) mediates spontaneous cytokine release from RA ex vivo synovial explant cultures. Signal transduction through TLRs controls the expression of a number of proinflammatory cytokines, including TNFα, IL-1 and IL-6, chemokines such as IL-8, and matrix metalloproteinases, factors that are spontaneously and chronically produced by dissociated RA synovial mononuclear cell cultures [2,3].
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