Abstract
Psoriasis vulgaris is a chronic, immune-mediated, inflammatory, polygenic skin disorder affecting approximately 2% of the population. It has a great impact on quality of life; patients often experience depression, anxiety, stigma as well as suicidal behavior. Even though psoriasis is one of the most studied dermatological conditions, the pathogenesis of the disease is still not completely elucidated. The complex interactions between keratinocytes, dendritic cells, T-lymphocytes, neutrophils and mast cells are responsible for the histopathological changes seen in psoriasis. The pathogenic model leading to the formation of psoriatic plaques has however evolved a lot over the years. There is now enough evidence to support the role of interleukin (IL) -23, IL-17, IL-22, T helper (Th) -17 cells, Th-22 cells, T regulatory cells, transforming growth factor (TGF)-β1 and IL-10 in the pathogenesis of the disease. Moreover, several inflammatory and anti-inflammatory molecules are currently being investigated, some of them showing promising results. The aim of this paper is to look over the most recent advances in the immunological pathways involved in the pathogenesis of psoriasis vulgaris.
Highlights
Psoriasis vulgaris is a chronic, immune-mediated, inflammatory, polygenic skin disorder affecting approximately 2% of the population
The aim of this paper is to look over the most recent advances in the immunological pathways involved in the pathogenesis of psoriasis vulgaris
In a study performed on 60 patients with psoriasis and 30 healthy controls, the authors found significantly higher levels of IL-6, IL-20 and IL-22 in psoriatic patients than in the control group, the concentrations of IL-20 and IL-22 being positively correlated with disease severity measured with psoriasis area and severity index (PASI) and body surface area (BSA)
Summary
Psoriasis vulgaris is a chronic, immune-mediated, inflammatory, polygenic skin disorder affecting approximately 2% of the population. It has a universal occurrence; males and females being affected [1,2,3,4]. While the disease was initially considered an epidermal disorder in which various mediators like cyclic adenosine monophosphate, protein kinase C, phospholipase C, eicosanoids, transforming growth factor (TGF)-α had a central role [6,7], in later years the role of T-cells was recognized and interferon (IFN)-γ and interleukin (IL)-12 were considered key players in the pathogenesis of psoriasis [12]. The aim of this paper is to look over the most recent advances in the immunological pathways involved in the pathogenesis of psoriasis vulgaris
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