Doina Diaconu

TL;DR: A role for IL-17C in skin inflammation is identified and a pathogenic function for the elevated IL-18C observed in lesional psoriasis skin is suggested, suggesting that IL- 17C, when coupled with other proinflammatory signals, initiates the development of psoriasiform dermatitis.

TL;DR: It is demonstrated that sensory nerve-derived peptides mediate psoriasiform dendritic cell and T cell infiltration and acanthosis and introduce targeting nerve-immunocyte/keratinocyte interactions as potential psoriasis therapeutic treatment strategies.

TL;DR: It is shown that IMQ does not uniquely model psoriasis but in fact triggers a core set of pathways active in diverse skin diseases, and suggests that B6 mice provide a better background than other strains for modeling Psoriasis disease mechanisms.

TL;DR: It is demonstrated that sustained skin-specific inflammation promotes aortic root inflammation and thrombosis and suggested that aggressive treatment of skin inflammation may attenuate pro-inflammatory and prothrombotic pathways that produce cardiovascular disease in psoriasis patients.

TL;DR: In this article, the authors showed that Tie2 expression is confined to either endothelial cells or keratinocytes, and confining Tie2 overexpression solely to keratinocyte results in a mouse model that meets the clinical, histological, immunophenotypic, biochemical, and pharmacological criteria required for an animal model of human psoriasis.