Abstract
Psoriasis is characterized by an apoptosis-resistant and metabolic active epidermis, while a hallmark for allergic contact dermatitis (ACD) is T cell-induced keratinocyte apoptosis. Here, we induced ACD reactions in psoriasis patients sensitized to nickel (n = 14) to investigate underlying mechanisms of psoriasis and ACD simultaneously. All patients developed a clinically and histologically typical dermatitis upon nickel challenge even in close proximity to pre-existing psoriasis plaques. However, the ACD reaction was delayed as compared to non-psoriatic patients, with a maximum intensity after 7 days. Whole genome expression analysis revealed alterations in numerous pathways related to metabolism and proliferation in non-involved skin of psoriasis patients as compared to non-psoriatic individuals, indicating that even in clinically non-involved skin of psoriasis patients molecular events opposing contact dermatitis may occur. Immunohistochemical comparison of ACD reactions as well as in vitro secretion analysis of lesional T cells showed a higher Th17 and neutrophilic migration as well as epidermal proliferation in psoriasis, while ACD reactions were dominated by cytotoxic CD8+ T cells and a Th2 signature. Based on these findings, we hypothesized an ACD reaction directly on top of a pre-existing psoriasis plaque might influence the clinical course of psoriasis. We observed a strong clinical inflammation with a mixed psoriasis and eczema phenotype in histology. Surprisingly, the initial psoriasis plaque was unaltered after self-limitation of the ACD reaction. We conclude that sensitized psoriasis patients develop a typical, but delayed ACD reaction which might be relevant for patch test evaluation in clinical practice. Psoriasis and ACD are driven by distinct and independent immune mechanisms.
Highlights
Psoriasis and allergic contact dermatitis (ACD) are highly prevalent, complex inflammatory skin diseases characterized by a combination of epithelial alterations and deviated T cell immunity [1,2].In recent years, substantial progress was made in understanding the pathogenesis of both psoriasis and ACD
We demonstrate that psoriasis patients can develop delayed, but otherwise typical contact dermatitis
Contact dermatitis is delayed in psoriasis patients As a first step to investigate whether sensitized psoriasis patients develop a typical ACD reaction, we performed nickel patch tests in patients with plaque-type psoriasis and a known hypersensitivity reaction to nickel (n = 14)
Summary
Psoriasis and allergic contact dermatitis (ACD) are highly prevalent, complex inflammatory skin diseases characterized by a combination of epithelial alterations and deviated T cell immunity [1,2].In recent years, substantial progress was made in understanding the pathogenesis of both psoriasis and ACD. Psoriasis and allergic contact dermatitis (ACD) are highly prevalent, complex inflammatory skin diseases characterized by a combination of epithelial alterations and deviated T cell immunity [1,2]. Previous attempts to do so were limited by high interindividual variability caused by different genetic background as well as environmental exposure, skin infections or trauma and eventual systemic or topical treatments [7,8,9]. These obstacles may largely be overcome by the possibility to investigate both diseases in the same patient at the same time. A prerequisite for general conclusions from such an analysis is the proof that sensitized psoriasis patients develop typical dermatitis either spontaneously [10] or to iatrogenic epicutaneous challenge with allergens or haptens (ACD), respectively
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