Modulation of inflammatory gene transcripts in psoriasis vulgaris: Differences between ustekinumab and etanercept

Since the advent of biologic therapy for psoriasis in 2003, continued development of cytokine antagonists has yielded progressively better clinical outcomes, as assessed using the Psoriasis Area and Severity Index (PASI) or Patient's Global Assessment. In addition, more targeted therapies seemingly afford better patient adherence. For example, the anti–IL-12/23 mAb ustekinumab has demonstrated much better “drug survival” than the TNF antagonists etanercept and adalimumab.1 Previous molecular profiling showed that etanercept strongly suppressed genes associated with the IL-23/type 17 T-cell pathway and psoriasis disease transcriptome (PSTR), but patients with resolved lesions retained expression of certain inflammatory genes (“molecular scar”) of psoriasis that could potentially reignite pathogenic skin inflammation on drug discontinuation.