Langerhans cell markers CD1a and CD207 are the most rapidly responding genes in lesional psoriatic skin following adalimumab treatment.

TNFα-, IL-23- and IL-17-targeting drugs are highly effective in the treatment of psoriasis. However, the precise molecular mechanism remains unknown. In psoriatic skin, the presence of Langerhans cells (LCs) is reduced, but the role of LC is poorly understood.

IL-17F regulates psoriasis-associated genes through IκBζ.

Psoriasis is a common chronic inflammatory and immune-mediated skin disease. Antagonists of TNF-α and, recently, IL-17 have proven to be highly effective in the treatment for psoriasis; however, the molecular mechanisms involved in the pathogenesis of psoriasis are poorly understood. Recently, we presented evidence that IκBζ is a key regulator in the development of psoriasis through its role in mediating IL-17A-driven effects.

Pro-inflammatory cytokine release in keratinocytes is mediated through the MAPK signal-integrating kinases.

The mitogen-activated protein kinases (MAPKs) are known to play a key role in the regulation of cytokine expression in several cell types. MAPK signal-integrating kinase 1 (Mnk1) is a kinase activated through both the stress- and cytokine-activated p38 MAPK pathway and the classical extracellular signal-regulated kinase 1/2 (ERK1/2) pathway. In this study, we demonstrate that in cultured normal human keratinocytes Mnk1 and its downstream target eukaryotic initiation factor 4E (eIF4E) are phosphorylated in a time-dependent manner in response to stimulation with anisomycin or interleukin (IL)-1beta.