Comparative studies of adherent rheumatoid synovial cells in primary culture: characterisation of the dendritic (stellate) cell.
Primary cultures of adherent rheumatoid synovial cells contain variable proportions of fibroblasts, macrophages, and dendritic cells, as judged by morphological appearance. Comparative studies using various enzymic and histochemical staining procedures showed the dendritic cells to lack many of the characteristic features of macrophages, e.g. the failure to express HLA-DR (Ia) antigen. The dendritic cells and fibroblasts had several similarities, but differed to some extent in their nonspecific esterase activity, phagocytic and proliferative potential. As the proportions of dendritic cells and fibroblasts varied in relation to specific culture conditions, we examined the possibility that these morphologies might represent different functional states rather than distinct cellular origins. Using subcultured synovial fibroblasts with a uniform bipolar appearance, we have shown that exposure to interleukin-1 or mast cell products resulted in a transformation to dendritic morphology. This change in cell shape was prevented by the presence of indomethacin, but was subsequently achieved by the addition of exogenous PGE2. Thus it appears that the latter is the factor that modulates the morphological change of fibroblastic to dendritic cells. This study has also demonstrated the complete and reversible interchange of fibroblast/dendritic morphology, thereby confirming that these different shapes are manifest by the same cell. The changes in phenotypic expression associated with the dendritic appearance include increased production of collagenase, prostaglandin E, and nonspecific esterase, as well as an apparent inability to exhibit phagocytosis and to proliferate in culture. We conclude from our in vitro studies that the phenotypic behaviour of the synovial fibroblast (or synoviocyte) is very variable and dependent to a large extent upon local stimuli, but the identity and hierarchy of such stimulating and suppressive factors in relation to cellular interactions requires further study.
D000954:Antigens, Surface / Q000032:analysis; D001172:Arthritis, Rheumatoid / Q000473:pathology*; D002448:Cell Adhesion; D002478:Cells, Cultured; D003713:Dendritic Cells / Q000187:drug effects / Q000473:pathology*; D015232:Dinoprostone; D004950:Esterases / Q000378:metabolism; D005347:Fibroblasts / Q000187:drug effects / Q000473:pathology; D006684:HLA-DR Antigens / Q000032:analysis; D006651:Histocytochemistry; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D007375:Interleukin-1 / Q000502:physiology; D008264:Macrophages / Q000187:drug effects / Q000473:pathology; D008407:Mast Cells / Q000502:physiology; D011458:Prostaglandins E / Q000494:pharmacology; D013583:Synovial Membrane / Q000473:pathology*
D000954:Antigens, Surface; D006684:HLA-DR Antigens; D007375:Interleukin-1; D011458:Prostaglandins E; D004950:Esterases; D015232:Dinoprostone; D007213:Indomethacin