Lifting the silver flakes: the pathogenesis and management of chronic plaque psoriasis

Abstract

Psoriasis is a common chronic inflammatory skin condition in which patients suffer from mild to chronic plaque skin plaques. The disease manifests through an excessive inflammatory response in the skin due to complex interactions between different genetic and environmental factors. Psoriasis can affect the physical, emotional, and psychosocial well-being of patients, and currently there is no cure with treatments focusing primarily on the use of anti-inflammatory agents to control disease symptoms. Traditional anti-inflammatory agents can cause immunosuppression and adverse systemic effects. Further understanding of the disease has led to current areas of research aiming at the development of selective molecular targets to suppress the pathogenic immune responses.

Figure 1

Clinical and histological appearance of stable chronic psoriatic plaques. Note the well-demarcated erythematous plaques covered by white-silvery scales distributed on the lower back (a), extremities (b), and scalp (c). Histological appearance of the chronic psoriatic plaque (d) reveals acanthosis (white arrow head), elongated epidermal rete ridges (two-headed arrow), and hyperkeratosis (black arrow head). Inflammatory cells are present in the dermis (long arrow) and sometimes in the epidermis known as Munro's microabscess which are composed of neutrophils (short arrow).

Figure 2

Contribution of both acquired and innate immunity to the pathogenesis of psoriasis. Acquired immunity leads to a T-cell activation and differentiation in response to different inflammatory signals while the innate immunity responds to a local tissue damage and proinflammatory cytokines production which in combination with nucleic acids from dying keratinocytes trigger the activation of TLR 8 and TLR 9 in myeloid DCs and plasmacytoid DCs, respectively. The interplay between the keratinocytes and immune mediators contributes to the formation of a self-perpetuating loop. IL: interleukin; IFN: interferon; TGF: transforming growth factor; TNF: tissue necrosis factor; pDC: plasmacytoid dendritic cell; mDC: myeloid dendritic cell; TLR: Toll-like receptor.