Psoriasis is a chronic inflammatory disease of skin and joints affecting approximately 1-2% of the population worldwide. In 2016, the WHO released a global report on psoriasis as one of the common serious noncommunicable diseases. Patients with psoriasis vulgaris present with scaly, erythematous plaques on the skin. The psoriatic skin lesions are characterized by an infiltration with immune cells, accelerated proliferation of keratinocytes and endothelial cells. The disease is considered to be a T cell-mediated autoimmune disease. For more than one decade, interferon-gamma (IFN-γ)-producing T helper (Th) 1 cells were thought to be the main drivers of psoriasis pathogenesis [1]. T cells isolated from psoriatic plaques of patients were capable to produce IFN-γ and patients with psoriatic arthritis receiving recombinant IFN-γ in clinical studies developed psoriatic lesions at injection sites [2, 3]. Over the past years our understanding of the cellular and molecular mechanisms underlying psoriasis has markedly improved. Nowadays, psoriasis is considered primarily a Th17-driven disease with increased levels of interleukin (IL-) 17A, IL-22 and IL-23. The antimicrobial peptide LL37 and the melanocytic peptide ADAMTS-like protein 5 have been reported as putative autoantigens in psoriasis with the potential to induce IL-17A expression by reactive T cells [4, 5]. Th17-associated cytokines directly act on multiple immune and nonimmune cells and promote the typical characteristics of psoriatic skin [6]. Of note, several polymorphisms of genes encoding Th17-associated factors like IL-23 (IL23A), its receptor (IL23R), and related signaling proteins (TYK2, RUNX3, STAT3, REL, TRAF3IP2, CARD14) are all associated with psoriasis susceptibility. The IL4/IL13 gene locus is also linked to psoriasis [7]. This is of interest, since IL-4 and IL-13 are typically produced by Th2 cells, which are implicated in the pathogenesis of allergic and atopic diseases, but are almost absent in psoriatic plaques [1].