Tumor necrosis factor-alpha as a potential therapeutic target in idiopathic inflammatory myopathies.
The cytokine, tumor necrosis factor alpha (TNFα), has been implicated in many aspects of immune system development, immune response regulation, and T cell-mediated tissue injury. TNFα plays a less well-defined role in the pathogenesis of the idiopathic inflammatory myopathy (IIM) group of disorders, and has been considered a potential therapeutic target. Observational studies of TNFα-blockade in (mostly refractory) IIM have yielded inconsistent beneficial results so that administration of these biological agents is presently deemed an unreliable alternative treatment strategy. Moreover, anti-TNFα therapy has the rare potential to trigger myositis in patients with rheumatoid arthritis, hinting at a pre-existing "overlap disorder". The full potential of TNFα-antagonism will be realized only if randomized controlled trials ascertain appropriate treatment regimens and identify patient subgroups most likely to benefit from such therapy.
Department of Neurology and Neuroscience, Weill Cornell Medical College/New York-Presbyterian Hospital, 525 East 68th Street, New York, NY 10065-4885, USA. pstuebge@med.cornell.edu
Joerg-Patrick
JP
Stübgen
D000328:Adult; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009220:Myositis / Q000188:drug therapy*; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000627:therapeutic use*; D055815:Young Adult
D000893:Anti-Inflammatory Agents; D014409:Tumor Necrosis Factor-alpha
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