Background: TNF-like molecule 1A (TL1A) is a ligand of the tumor necrosis factor (TNF) superfamily that mediates apoptosis and inflammation via its effective receptor DR3 and the activation of NF-κB. Toll-like receptors (TLRs) are receptors that recognize microbes and activate the immune response. Endogenous ligands such as interleukin 1β (IL-1β) and fibronectin fragments also trigger the TLR2-mediated immune response. Recently, the DR3 receptor was found in the synovia of patients with rheumatoid arthritis and osteoarthritis. In this study, we examined the influence of TL1A on the expression of TLRs 1-5 in synovial fibroblasts. Methods: Synovial fibroblasts were isolated from rat knee joints and treated with TL1A for 0, 6, 12, or 24 h. Changes in TLR 1-5 expression were determined by RT-PCR. The expression of TLR2 protein was detected by immunocytochemistry and western blotting. Results: The expression of the Tlr2 was significantly upregulated by TL1A in the first six hours of stimulation. TLR2 protein was also upregulated. The expression of Tlr1 and Tlr3-5 was not significantly affected by TL1A. Conclusions: We have demonstrated for the first time that TLR2 expression is upregulated by TL1A in synovial fibroblasts. DR3 expression in rheumatoid arthritis and osteoarthritis and our findings suggest that TL1A plays a role in the process of articular inflammation and somehow influences the expression of TLR2.
|頁（從 - 到）
|Journal of Medical Sciences (Taiwan)
|已發佈 - 2月 2008
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