Advances in Understanding the Immunological Pathways in Psoriasis

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.

Keywords: IL-17; T regulatory cells; Th-17; immunology; inflammation; psoriasis.

Figure 1

Cytokine network in psoriasis. IFNα  =  interferon-α, IFNγ  =  interferon-γ, IL-6 = interleukin-6, IL-8  =  interleukin-8, IL-12  =  interleukin-12, IL-17  =  interleukin-17, IL-22  =  interleukin-22, IL-23  =  interleukin 23, LL37 = cathelicidin, PMN  =  polymorphonuclears, S 100 = S 100 proteins, Th1  =  T helper 1, Th17  =  T helper 17, Th22 = T helper 22, TGFβ  =  transforming growth factor-beta, Tn  =  naïve T lymphocyte, TNFα  =  tumor necrosis factor-α, and TNFβ  =  tumor necrosis factor-β.