Cytokines and oncogenes in cellular interactions of rheumatoid arthritis.
Rheumatoid arthritis (RA) is a chronic systemic disorder of unknown etiology. Most of its debilitation sequelae are derived from progressive destruction of joints. The affected joints exhibit inflammation, abnormal immune responses and synovial hyperplasia. Although growth factors and cytokines derived from macrophages and endothelial cells contribute to the perpetuation of the inflammatory process, activated transformed-appearing synovial fibroblasts mediate cartilage and bone destruction. Based on the observation that synovial hyperplasia is associated with a transformed-appearing phenotype and an upregulated expression of protooncogenes and matrix degrading enzymes, the present studies are designed to explore the role of a heretofore unknown (retro) virus-like particle in the pathogenesis of RA.
Keyszer
G M
GM
Department of Medicine, University of Alabama at Birmingham 35294.
Heer
A H
AH
Gay
S
S
D001172:Arthritis, Rheumatoid / Q000209:etiology* / Q000235:genetics; D002450:Cell Communication; D016207:Cytokines / Q000502:physiology*; D004790:Enzyme Induction / Q000235:genetics; D005347:Fibroblasts / Q000378:metabolism; D005786:Gene Expression Regulation; D006801:Humans; D008264:Macrophages / Q000378:metabolism; D008666:Metalloendopeptidases / Q000235:genetics / Q000502:physiology; D010641:Phenotype; D011519:Proto-Oncogenes / Q000235:genetics; D013583:Synovial Membrane / Q000473:pathology
D016207:Cytokines; D008666:Metalloendopeptidases