Psoriasis is a chronic inflammatory skin disease of unknown etiology that affects approximately 2-3% of the population. Psoriasis is characterized by the development of psoriatic plaques which can affect the whole body of patients and thus psoriasis can severely impair the quality of life. Hallmarks of the disease include the increased proliferation of keratinocytes, an inflammatory immune infiltrate and the induction of pro-inflammatory mediators in affected skin. Among the immune cells that infiltrate psoriatic skin lesions are plasmacytoid dendritic cells (pDCs), which are involved in the pathogenesis of human psoriasis due to their capacity to produce vast amounts of type I interferons (IFNs). In this thesis, I aimed at elucidating the role of pDCs in a mouse model of psoriasis-like skin inflammation by employing the imiquimod (IMQ) mouse model of psoriasiform dermatitis. IMQ is an agonist of toll-like receptor 7/8 (TLR7/8), a pattern recognition receptor (PRR) that recognizes single stranded RNA. Repeated topical application of IMQ on mouse skin induces a skin inflammation which resembles the phenotypic features of human psoriasis. I could show that FNAR1-/- mice develop a skin inflammation comparable to WT mice, suggesting that type I IFNs are dispensable for the development of skin inflammation in the IMQ model. In order to delineate the function of pDCs, I employed Bdca2-DTR transgenic mice to transiently deplete pDCs following diphtheria toxin (DT) injections. Interestingly, pDC ablation aggravated the skin inflammation instigated by topical IMQ application and the inflammation persisted during the resolution phase after IMQ withdrawal. The exacerbated IMQ-induced skin inflammation in pDC-depleted mice was accompanied by an altered cutaneous immune infiltrate consisting of increased numbers of monocytes, neutrophils and dermal gamma delta T cells (TCs). Moreover, compared to controls various pro-inflammatory cytokines were up-regulated in the skin of IMQ treated and pDC-depleted mice. I could furthermore show that the frequency of IL-17 producing dermal TCs, which have been shown to drive the IMQ-induced skin inflammation, was increased in the skin of pDC-ablated mice. Together, these data suggest an immunosuppressive role of pDCs in the IMQ mouse model of psoriasiform dermatitis. In fact, I discovered that pDCs up-regulate programmed death-ligand 1 (PD-L1) in the skin as well as in skin draining lymph nodes upon IMQ application. Additionally, dermal TCs expand during IMQ treatment and up-regulate the cognate inhibitory receptor PD-1. By employing a co-culture system, I was able to show that IMQ stimulated pDCs inhibit the production of IL-17 by TCs via PD-1-PD-L1 engagement, since incubation with PD-L1 blocking antibodies restored IL-17 production. Consequently, PD-L1 blockade by the administration of PD-L1 blocking antibodies exacerbated the IMQ-induced skin inflammation in vivo. In summary, my work has revealed a novel mechanism by which pDCs elicit immunosuppressive properties following IMQ treatment involving up-regulation of PD-L1, which restrains exacerbated IL-17 production in TCs.