Cloning of follistatin-related protein as a novel autoantigen in systemic rheumatic diseases.

作者: Masao Tanaka , Shoichi Ozaki , Fumio Osakada , Kiyoshi Mori , Mitsuo Okubo

DOI: 10.1093/INTIMM/10.9.1305

关键词:

摘要: In an attempt to identify autoantigens of synovium in rheumatoid arthritis (RA), we constructed lambda phage expression cDNA libraries from and screened them by IgG purified synovial fluids, both which were derived RA patients. As a result this unique combination the probes, cloned follistatin-related protein (FRP) as novel autoantigen systemic rheumatic diseases. FRP is secreted containing similar amino acid sequence follistatin, inhibitor activin. was first transforming growth factor-beta1-inducible (called TSC-36) mouse osteoblastic cell line suggested have some roles negative regulation cellular growth. Immunoblotting analyses detected fluid serum anti-FRP antibodies class more frequently than any other diseases controls. Synovial appeared 44% (n = 18) none osteoarthritis (OA) 15) Serum 30% 67), 17% sclerosis 18), 10% lupus erythematosus 51) Sjogren's syndrome 10), polymyositis/dermatomyositis 13) patients healthy subjects 30). These recognized EC domain, extracellular Ca2+ binding module. antibody-positive patients, C-reactive level erythrocyte sedimentation rate elevated (P < 0.05 P 0.01, respectively). gene higher OA 0.05). However, there no difference between these groups amount FRP, suggesting its turnover RA. follistatin inhibits activin, might inhibit factor-like molecule. Detection antibodies, possibly having disease-promoting effects blocking could be one markers for clinical evaluation

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