International Immunology, Vol 10, 1305-1314, Copyright © 1998 by Oxford University Press
M Tanaka, S Ozaki, F Osakada, K Mori, M Okubo and K Nakao
In an attempt to identify autoantigens of synovium in rheumatoid arthritis
(RA), we constructed lambda phage expression cDNA libraries from synovium
and screened them by IgG purified from synovial fluids, both of which were
derived from RA patients. As a result of this unique combination of the
libraries and probes, we cloned follistatin-related protein (FRP) as a
novel autoantigen in systemic rheumatic diseases. FRP is a secreted protein
containing a similar amino acid sequence to follistatin, an inhibitor of
activin. FRP was first cloned as a transforming growth
factor-beta1-inducible protein (called TSC-36) from a mouse osteoblastic
cell line and was suggested to have some roles in the negative regulation
of cellular growth. Immunoblotting analyses detected synovial fluid and
serum anti-FRP antibodies of IgG class more frequently in RA than any other
systemic rheumatic diseases and controls. Synovial fluid anti-FRP
antibodies appeared in 44% of RA (n = 18) and none of osteoarthritis (OA)
(n = 15) patients. Serum antibodies were detected in 30% of RA (n = 67),
17% of systemic sclerosis (n = 18), 10% of systemic lupus erythematosus (n
= 51) and Sjogren's syndrome (n = 10), and none of
polymyositis/dermatomyositis (n = 13) patients and healthy subjects (n =
30). These antibodies recognized an EC domain, an extracellular Ca2+
binding module. In anti-FRP antibody- positive RA patients, serum
C-reactive protein level and erythrocyte sedimentation rate were more
elevated than negative patients (P < 0.05 and P < 0.01,
respectively). FRP gene expression was higher in RA than OA synovium (P
< 0.05). However, there was no difference between these groups in the
amount of synovial FRP, suggesting its elevated turnover in RA. As
follistatin inhibits activin, FRP might inhibit some growth factor-like
molecule. Detection of anti-FRP antibodies, possibly having
disease-promoting effects as the blocking antibodies, could be one of the
markers for clinical evaluation of systemic rheumatic diseases.
ARTICLES
Cloning of follistatin-related protein as a novel autoantigen in systemic rheumatic diseases
Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, Japan.
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