Tumor-necrosis factor-α induces retinoic acid-inducible gene-I in rheumatoid fibroblast-like synoviocytes

Abstract

Tumor-necrosis factor-α (TNF-α) is a potent proinflammtory cytokine and a key molecule in the pathogenesis of rheumatoid arthritis (RA). Retinoic acid-inducible gene-I (RIG-I) is a DExH box protein, which is known to play a role in the inflammatory and immune reactions. We previously reported about potential involvement of RIG-I in synovial inflammation in RA. In the present study, we demonstrated the expression of RIG-I in fibroblast-like synoviocytes stimulated with TNF-α. RNA interference against interferon (IFN)-β abolished the TNF-α-induced RIG-I expression. In addition, knockdown of RIG-I partially inhibited the TNF-α-induced expression of CC chemokine ligand (CCL) 5, a chemokine with chemotactic activity toward lymphocytes and monocytes. These findings suggest that the TNF-α/IFN-β/RIG-I/CCL5 pathway may be involved in the pathogenesis of synovial inflammation in RA.