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Psoriasis often responds to treatment with tumor necrosis factor (TNF) inhibitors produced by Th1 helper cells. Also successful are treatments that block Th17 cell activation by the p40 cytokine subunits of interleukins IL-12 and IL-23. In other words, blocking either pathway halts events leading to development and maintenance of the psoriatic plaque. This evidence suggests that the anti-TNF and anti-Th17 pathways interconnect. In a recent study, investigators studied gene arrays in patients whose psoriasis was being treated with the TNF inhibitor etanercept, looking for differences in responders and nonresponders.
Cluster analysis defined gene sets in these patients that modulated over the 12-week treatment period. Four clusters of downregu…