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.