[Possible pathogenesis of rheumatoid arthritis].
Rheumatoid fibroblast-like synoviocytes characteristically proliferate in an anchorage-independent manner, and are deeply implicated in cartilage destruction. Our previous results showed that rheumatoid synoviocytes expressed Fas ligand and were induced apoptosis by anti-Fas antibody treatment. In addition, several transcriptional factors, such as NF kappa B and AP-1 significantly activated in rheumatoid synoviocytes. We are now clarifying the pathogenesis of RA with the method, yeast two-hybrid system as 'post genome' strategy. We recently found that several factors that related with cell differentiation highly expressed in rheumatoid synoviocytes. In this report we discuss possible pathogenesis of RA based on our recent data and application to the therapy tool against RA.
Nakazawa
M
M
Rheumatology, Immunology and Genetics Program, Institute of Medical Science, St. Marianna University School of Medicine.
Nakajima
T
T
Nishioka
K
K
D017209:Apoptosis; D001172:Arthritis, Rheumatoid / Q000209:etiology / Q000235:genetics; D050882:CREB-Binding Protein; D016045:Human Genome Project; D006801:Humans; D008565:Membrane Proteins / Q000502:physiology; D009687:Nuclear Proteins / Q000502:physiology; D051881:Receptor, Notch1; D011956:Receptors, Cell Surface; D013583:Synovial Membrane / Q000166:cytology; D015534:Trans-Activators / Q000502:physiology; D014157:Transcription Factors / Q000378:metabolism
D008565:Membrane Proteins; C497761:NOTCH1 protein, human; D009687:Nuclear Proteins; D051881:Receptor, Notch1; D011956:Receptors, Cell Surface; D015534:Trans-Activators; D014157:Transcription Factors; D050882:CREB-Binding Protein; C494363:CREBBP protein, human