T cell-independent cellular pathways of rheumatoid joint destruction.
An appreciation of the role of T cell-independent pathways in the pathogenesis of rheumatoid arthritis (RA) has led to significant advances. New approaches have included the identification of novel cytokines and growth factors and characterization of the recently defined chemokines. Greater insight has been achieved with regard to prostaglandin pathways and the role of the synovial matrix and vasculature. The synovial matrix contributes to cell regulation in RA to a greater extent than previously believed, and the vasculature of the synovium must now be regarded as an active participant in the regulation of cell growth. The most exciting development, however, is the recognition of the involvement of oncogenes and apoptosis pathways in the dysregulation of the synovial cell cycle, which presumably causes the continuous synovial growth that is characteristic of RA.
Müller-Ladner
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Department of Medicine, University of Alabama at Birmingham 35294-0006, USA.
D017209:Apoptosis / Q000502:physiology; D001172:Arthritis, Rheumatoid / Q000209:etiology / Q000473:pathology*; D002450:Cell Communication / Q000502:physiology; D002455:Cell Division; D006801:Humans; D007596:Joints / Q000378:metabolism / Q000473:pathology*; D011453:Prostaglandins / Q000378:metabolism; D011519:Proto-Oncogenes; D013583:Synovial Membrane / Q000098:blood supply / Q000473:pathology*; D013601:T-Lymphocytes / Q000502:physiology*
D011453:Prostaglandins