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We read with interest the report by Drynda et al demonstrating that treatment of rheumatoid arthritis (RA) with anti-tumour necrosis factor α (anti-TNFα) induces subtle changes in the cytokine network such as down regulation of the proinflammatory cytokine interleukin 6 (IL6), but does not affect the persistently high plasma levels of transforming growth factor β (TGFβ).1 Furthermore, they suggest that the latter finding indicates the existence of as yet unknown mechanisms for TGFβ overexpression in RA that may predispose a patient to severe infections and altered tumour defence.
Complementary to the observations noted above are our findings using DNA microarray in patients with RA treated with TNF antagonists as compared with patients with RA treated with methotrexate and healthy controls.2 A total of 12 000 genes were analysed (human genome U 95 A Array-Affimetrix) and a variety of gene functions, including apoptosis, transcription factors, cell …