bay-11-7082 and pristane

bay-11-7082 has been researched along with pristane* in 1 studies

Other Studies

1 other study(ies) available for bay-11-7082 and pristane

Article	Year
Pristane primed rat T cells enhance TLR3 expression of fibroblast-like synoviocytes via TNF-α initiated p38 MAPK and NF-κB pathways. Clinical immunology (Orlando, Fla.), 2015, Volume: 156, Issue:2 Based on pristane-induced arthritis (PIA), we found that T cells mediate TLR3 overexpression in fibroblast-like synoviocytes (FLS). The aim of this study is to determine key factors by which T cells induce TLR3 expression. Rat FLS were co-cultured with pristane primed T cell conditioned medium (PPT medium), and TLR3 expression of FLS was significantly induced. TNF-α, IFN-γ and IL-17 were dominantly expressed in PIA T cells. The overexpression of TLR3 and its related genes in FLS co-cultured with PPT medium could be reduced through blocking TNF-α pathway. CD4(+) T cells from spleen of PIA rats showed increase of TNF-α secretion. P38 MAPK and NF-κB were activated in FLS by PPT medium, and their inhibitors decreased TLR3 upregulation significantly. Finally, TNF-α induced TLR3 expression was confirmed in human synovial cells. Summarily, TNF-α derived from pristane primed T cells induced TLR3 expression of FLS through activating p38 MAPK and NF-κB pathways. Topics: Animals; Arthritis, Experimental; CD4-Positive T-Lymphocytes; Cell Line; Culture Media, Conditioned; Enzyme Inhibitors; Humans; Imidazoles; Immunosuppressive Agents; Interferon-gamma; Interleukin-17; Interleukin-6; Matrix Metalloproteinase 13; Matrix Metalloproteinase 3; NF-kappa B; Nitriles; p38 Mitogen-Activated Protein Kinases; Pyridines; Rats; RNA, Messenger; Sulfones; Synovial Membrane; Terpenes; Toll-Like Receptor 3; Tumor Necrosis Factor-alpha; Up-Regulation	2015

Article

Year

Pristane primed rat T cells enhance TLR3 expression of fibroblast-like synoviocytes via TNF-α initiated p38 MAPK and NF-κB pathways.

Clinical immunology (Orlando, Fla.), 2015, Volume: 156, Issue:2

Based on pristane-induced arthritis (PIA), we found that T cells mediate TLR3 overexpression in fibroblast-like synoviocytes (FLS). The aim of this study is to determine key factors by which T cells induce TLR3 expression. Rat FLS were co-cultured with pristane primed T cell conditioned medium (PPT medium), and TLR3 expression of FLS was significantly induced. TNF-α, IFN-γ and IL-17 were dominantly expressed in PIA T cells. The overexpression of TLR3 and its related genes in FLS co-cultured with PPT medium could be reduced through blocking TNF-α pathway. CD4(+) T cells from spleen of PIA rats showed increase of TNF-α secretion. P38 MAPK and NF-κB were activated in FLS by PPT medium, and their inhibitors decreased TLR3 upregulation significantly. Finally, TNF-α induced TLR3 expression was confirmed in human synovial cells. Summarily, TNF-α derived from pristane primed T cells induced TLR3 expression of FLS through activating p38 MAPK and NF-κB pathways.

Topics: Animals; Arthritis, Experimental; CD4-Positive T-Lymphocytes; Cell Line; Culture Media, Conditioned; Enzyme Inhibitors; Humans; Imidazoles; Immunosuppressive Agents; Interferon-gamma; Interleukin-17; Interleukin-6; Matrix Metalloproteinase 13; Matrix Metalloproteinase 3; NF-kappa B; Nitriles; p38 Mitogen-Activated Protein Kinases; Pyridines; Rats; RNA, Messenger; Sulfones; Synovial Membrane; Terpenes; Toll-Like Receptor 3; Tumor Necrosis Factor-alpha; Up-Regulation

2015