Expression data (U133 Plus 2.0) from fibroblast like synoviocytes from patients with rheumatoid arthritis (RA-FLS) stimulated by LIGHT.

LIGHT/TNFSF6, a member of the tumor necrosis factor (TNF) superfamily, can promote apoptosis in activated primary B cells, T cells, dendritic cells, and synovial fibroblasts through Fas and is involved in the pathogenesis of autoimmune diseases including rheumatoid arthritis (RA). Meanwhile, decoy receptor 3 (DcR3) competitively binds soluble LIGHT in addition to TL1A and FasL and inhibits the signaling of LIGHT via HEVN and. Therefore, LIGHT-DcR3/HEVN/ signaling may be involved in the pathogenesis of RA. We hypothesized that LIGHT regulates the gene expression in RA-FLS. We used to search for genes in which expression in RA-FLS is regulated by LIGHT. RA-FLS were obtained from 4 RA patients (sample1-4). Each sample was incubated with either 1.0 μg/ml recombinant human LIGHT protein or phosphate buffered saline diluted with serum-free Opti-MEM medium as non-stimulated control. Gene expression in RA-FLS stimulated by LIGHT was compared with that of their respective non-stimulated controls.