Psoriasis is one of the commonest chronic inflammatory disorders. Its cause is unknown, but a wealth of studies indicate that the disease results from a complex and dynamic interplay between genetic and environmental factors that trigger an excessive inflammatory response in the skin. Dendritic cells and effector T-cells are central in the development of the psoriastic lesion, and cytokines produced by these cells stimulate keratinocytes to proliferate and increase the migration of inflammatory cells into the skin, promoting epidermal hyperplasia and inflammation. Understanding the immunology of the psoriatic plaque has led to new therapeutic options and novel candidates for immunomodulation, and has changed the ways psoriatic patients are managed.

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