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International Immunology, Vol. 15, No. 1, pp. 71-77, January 2003
© 2003 Japanese Society for Immunology

FEATURED ARTICLE OF THE MONTH

Potential preventive effects of follistatin-related protein/TSC-36 on joint destruction and antagonistic modulation of its autoantibodies in rheumatoid arthritis

Masao Tanaka1, Shoichi Ozaki3, Daisuke Kawabata1, Masaaki Kishimura4, Fumio Osakada4, Mitsuo Okubo5, Masao Murakami1, Kazuwa Nakao2 and Tsuneyo Mimori1

1 Department of Rheumatology and Clinical Immunology, and 2 Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, 54 Shogoin-Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan 3 Division of Rheumatology and Allergy, Department of Internal Medicine, St Marianna University School of Medicine, 2-16-1 Sugao, Miyamae-ku, Kawasaki 216-8511, Japan 4 Takasago Research Laboratories, Kaneka Corp., 1-8 Miyamae-machi, Takasago-cho, Takasago-shi, Hyogo 676-8688, Japan 5 Blood Transfusion Service, Saitama Medical Center, Saitama Medical School, 1981 Tujido-Street, Kamoda, Kawagoe-City, Saitama 350-8550, Japan.

Correspondence to: S. Ozaki; E-mail: ozk{at}marianna-u.ac.jp
Transmitting editor: T. Saito

We previously reported that follistatin-related protein (FRP)/TSC-36 was one of the target antigens of autoantibodies in rheumatoid arthritis (RA) and that the appearance of serum autoantibodies to FRP correlated to disease activity in RA. However, the significance of FRP in autoimmunity remained to be explained due to the unknown function of FRP. Here, we disclose in part the function of FRP. Transforming growth factor (TGF)-ß augmented FRP gene expression in synovial cells. FRP reduced synovial production of matrix metalloproteinase (MMP)-1, MMP-3 and prostaglandin E2, potent agonists of joint destruction in RA. In contrast, autoantibodies to FRP from patients with RA increased their production by blocking FRP activity, probably in the autocrine system. Moreover, FRP down-regulated synovial expression of FOS (c-fos), which seemed responsible for the reduction in MMP-1 and MMP-3 caused by FRP. Therefore, FRP and its autoantibody can be regarded as defensive and offensive factors respectively in rheumatoid arthropathy. The major epitope of autoantibodies to FRP was mapped to the sequence LKFVEQNE (residues 169–176) and homologous sequences were found in proteins from Escherichia coli, Epstein–Barr virus, etc. FRP and its autoantibody may provide some clues to elucidate the process of disease development and a new approach to the design of therapeutics in RA.

Keywords: autoimmunity, autoantigens, c-fos, epitopes


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