Ustekinumab is an effective monoclonal Ab against the shared p40 subunit of IL-12 and IL-23, capable of resolving psoriasis, with reports of prolonged remissions. Via neutralizing IL-12 and IL-23, ustekinumab reduces Th17 cell and keratinocyte activation. Because patients on ustekinumab noticed reduced new-formation of plaques and Koebnerization of their skin, we hypothesized that ustekinumab treatment would modify epidermal triggering in uninvolved skin and via this mechanism contribute to prolonged clinical remissions. We therefore tested uninvolved epidermis in psoriasis patient before and after one injection of ustekinumab using tape-stripping. Furthermore, we monitored the effect of treatment on serum -defensin-2. Our findings imply that ustekinumab inhibits cutaneous triggering as assessed by induction of epidermal regenerative markers without affecting the epidermal antimicrobial responses. Serum -defensin-2 appeared an appropriate biomarker for clinical responsiveness to ustekinumab therapy.

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Nederlands Tijdschrift voor Dermatologie en Venereologie
Department of Dermatology

Baerveldt, E. M., Thio, B., & Prens, E. (2012). Effects of ustekinumab on non-affected psoriatic skin. Nederlands Tijdschrift voor Dermatologie en Venereologie, 22(2), 120–122. Retrieved from