A speculation on the pathogenesis of joint inflammation in rheumatoid arthritis
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چکیده
منابع مشابه
TWEAK and Fn14 expression in the pathogenesis of joint inflammation and bone erosion in rheumatoid arthritis
INTRODUCTION TNF-like weak inducer of apoptosis (TWEAK) has been proposed as a mediator of inflammation and bone erosion in rheumatoid arthritis (RA). This study aimed to investigate TWEAK and TWEAK receptor (Fn14) expression in synovial tissue from patients with active and inactive rheumatoid arthritis (RA), osteoarthritis (OA) and normal controls and assess soluble (s)TWEAK levels in the syno...
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From the College of Medical, Veterinary, and Life Sciences, University of Glasgow, Glasgow, United Kingdom (I.B.M.); and the Department of Internal Medicine 3, University of Erlangen–Nuremberg, Erlangen, Germany (G.S.). Address reprint requests to Dr. McInnes at the College of Medical, Veterinary, and Life Sciences, University of Glasgow, Level 4, Sir Graeme Davis Bldg., 120 University Pl., Gla...
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Rheumatoid arthritis (RA) is due to a combination of phagocytosis and anaphylaxis gone awry. Immune complexes create their havoc via Fc gamma III receptors that signal via the tyrosine phosphorylation immunoreceptor pathway. Anaphylatoxins, mainly C5a, signal via the MEK kinase cascade, and both engage in cross-talk via NF kappa B. Aspirin-III blocks signals sent by both: immune complexes via F...
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ژورنال
عنوان ژورنال: Arthritis & Rheumatism
سال: 1965
ISSN: 0004-3591,1529-0131
DOI: 10.1002/art.1780080212