Increased proliferation of human synovial fibroblasts treated with recombinant immune interferon.
Because immune lymphocytes are commonly found in inflamed rheumatoid synovium, we tested the hypothesis that immune or gamma-interferon, a product of activated lymphocytes, may modulate synovial cell growth. Using a cell culture model, we found that addition of gamma-interferon at 10 to 100 antiviral units/ml to cultures of human synovial fibroblasts or human foreskin fibroblasts resulted in a two- to threefold increase in proliferation, measured by incorporation of [3H]thymidine and cell number. The proliferative effect was abrogated if the gamma-interferon was neutralized with a specific monoclonal antibody. Increased proliferation induced by gamma-interferon was antagonized by all-transretinoic acid but was enhanced by prednisolone. Our data indicate that the T cell product, gamma-interferon, can directly modulate synovial cell function and suggest that this interaction may play a role in the proliferative lesion of rheumatoid arthritis.
D001172:Arthritis, Rheumatoid / Q000276:immunology / Q000473:pathology; D002455:Cell Division / Q000187:drug effects; D005347:Fibroblasts / Q000166:cytology* / Q000276:immunology; D006133:Growth Substances / Q000494:pharmacology*; D006367:HeLa Cells / Q000166:cytology; D006801:Humans; D007371:Interferon-gamma / Q000494:pharmacology*; D011239:Prednisolone / Q000494:pharmacology; D013583:Synovial Membrane / Q000166:cytology* / Q000276:immunology; D014212:Tretinoin / Q000494:pharmacology
D006133:Growth Substances; D014212:Tretinoin; D007371:Interferon-gamma; D011239:Prednisolone