Pathogenesis of rheumatoid arthritis.
This report gives a review on recent results of investigations of cellular aspects of inflammation. The role of macrophages and T-helper-cells with particular focus to the effects of the various mediators on their target cells will be discussed. Interleukin 1, Tumor Necrosis Factor, Interleukin 2, and Interferon as well as arachidonic acid metabolites contribute to the clinical findings of inflammation. We have to admit that the whole process of inflammation in rheumatic arthritis (RA) is not yet clear. For example we do not know in detail why RA is self perpetuating, why and when rheumatoid pannus occurs or under which circumstances immune complexes may cause the various organ manifestations. Recent findings are discussed.
Kolarz
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G
Ludwig-Boltzmann-Institut für Rheumatologie und Fokalgeschehen, Sozialversicherungsanstalt der gewerblichen Wirtschaft, Baden bei Wien.
D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000502:physiology; D001172:Arthritis, Rheumatoid / Q000276:immunology*; D006801:Humans; D007372:Interferons / Q000502:physiology; D007375:Interleukin-1 / Q000502:physiology; D007376:Interleukin-2 / Q000502:physiology; D008262:Macrophage Activation; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
D001095:Arachidonic Acids; D007375:Interleukin-1; D007376:Interleukin-2; D014409:Tumor Necrosis Factor-alpha; D016718:Arachidonic Acid; D007372:Interferons