Over the last decade it has become apparent that common pathogenic mechanisms are shared between many human chronic inflammatory diseases of unrelated pathology and manifestation. These mechanisms include common inflammatory networks that control tissue destructive and repair processes and their study is of major therapeutic potential as recently demonstrated for TNFα. Thus, early studies in rheumatoid arthritis defined TNFα as a major therapeutic target, the blockade of which was subsequently proved to be of great efficacy in the clinic. This paved the way for the successful blockade of TNFα in various other diseases including Crohns disease, psoriasis, spondyloarthropathies and juvenile arthritis, although no similar networks with anti-TNFα at their apex had previously been demonstrated. In this article, we review the current knowledge of the pathogenic mechanisms involved in rheumatoid arthritis and chronic obstructive pulmonary disease with particular emphasis on the role of inflammatory cytokines, chemokines, and tissue degrading enzymes as revealed by studies in the laboratory and the clinic. Direct comparison of these mechanisms may provide clues for a future therapy for these painful and incurable diseases.
Keywords: rheumatoid arthritis, chronic obstructive pulmonary disease, inflammation, cytokines, proteases, monoclonal antibody
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