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Involvement of retinoic acid-inducible gene-I in inflammation of rheumatoid fibroblast-like synoviocytes

By T Imaizumi, T Arikawa, T Sato, R Uesato, T Matsumiya, H Yoshida, M Ueno, S Yamasaki, T Nakajima, M Hirashima, K Sakata, Y Ishibashi, S Toh, C Ohyama and K Satoh


Interferon (IFN)-γ is a major cytokine that regulates T helper 1-type immune reactions and serves as an important mediator in the pathogenesis of autoimmune diseases. Retinoic acid-inducible gene-I (RIG-I) is an IFN-γ-inducible gene and known to be involved in the inflammatory and immune reactions. In the present study, we found high levels of RIG-I expression in synovial tissues of rheumatoid arthritis (RA), while the expression in osteoarthritis tissues was low. Treatment of cultured fibroblast-like synoviocytes with IFN-γ markedly induced the expression of RIG-I. Knockdown of RIG-I in fibroblast-like synoviocytes, with specific siRNA, resulted in the inhibition of the IFN-γ-induced expression of chemokine (C-X-C motif) ligand 10 (CXCL10)/IFN-γ-inducible protein-10 (IP-10), a chemokine with chemotactic activity towards T cells. These findings suggest that RIG-I may play an important role in the pathogenesis of synovial inflammation in RA, at least in part, by regulating the IFN-γ-induced expression of CXCL10/IP-10

Topics: Basic Immunology
Publisher: Blackwell Science Inc
OAI identifier: oai:pubmedcentral.nih.gov:2492896
Provided by: PubMed Central
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