Emata
Psoriasis is a complex autoimmune inflammatory disease that occurs in genetically susceptible individuals and presents with the development of inflammatory plaques on the skin (picture 1A-B). Although early concepts of the pathogenesis of psoriasis focused primarily on keratinocyte hyperproliferation, dysregulation of the immune system is now recognized as a critical event in this disease. The evolving knowledge of the role of the immune system in psoriasis has had a significant impact on treatment development. Many new and emerging therapeutic agents target specific immunologic aspects of psoriatic disease. (See"Treatment of psoriasis".)
The pathophysiology of psoriasis will be discussed here. The epidemiology, genetics, clinical features, diagnosis, and management of psoriasis are reviewed separately.
Involvement of the immune system in psoriasis was first indicated in early studies that identified complex infiltrates of leukocytes involved in both innate and adaptive immunity in psoriatic skin [1,2]. Subsequent studies have supported the concept that interactions between dendritic cells, T cells, keratinocytes, neutrophils, and the cytokines released from immune cells likely contribute to the initiation and perpetuation of the cutaneous inflammation that is characteristic of psoriasis [3]. A basic sequence of the immunologic events that are theorized to occur in psoriasis is described below [3]: * Antigenic stimuli contribute to the activation of plasmacytoid dendritic cells and other innate immune cells in the skin. * Proinflammatory cytokines produced by innate immune cells, including interferon (IFN)-alpha, stimulate the activation of myeloid dendritic cells in the skin. * Myeloid dendritic cells produce cytokines, such as interleukin (IL)-23 and IL-12 that stimulate the attraction, activation, and differentiation of T cells. * Recruited T cells produce cytokines that stimulate keratinocytes to proliferate and produce proinflammatory
The pathophysiology of psoriasis will be discussed here. The epidemiology, genetics, clinical features, diagnosis, and management of psoriasis are reviewed separately.
Involvement of the immune system in psoriasis was first indicated in early studies that identified complex infiltrates of leukocytes involved in both innate and adaptive immunity in psoriatic skin [1,2]. Subsequent studies have supported the concept that interactions between dendritic cells, T cells, keratinocytes, neutrophils, and the cytokines released from immune cells likely contribute to the initiation and perpetuation of the cutaneous inflammation that is characteristic of psoriasis [3]. A basic sequence of the immunologic events that are theorized to occur in psoriasis is described below [3]: * Antigenic stimuli contribute to the activation of plasmacytoid dendritic cells and other innate immune cells in the skin. * Proinflammatory cytokines produced by innate immune cells, including interferon (IFN)-alpha, stimulate the activation of myeloid dendritic cells in the skin. * Myeloid dendritic cells produce cytokines, such as interleukin (IL)-23 and IL-12 that stimulate the attraction, activation, and differentiation of T cells. * Recruited T cells produce cytokines that stimulate keratinocytes to proliferate and produce proinflammatory