Psoriasis is a chronically relapsing skin inflammation affecting about 2% the population worldwide. Plaque psoriasis, also known as psoriasis vulgaris, is the most common form of the disease. However there is now accumulating evidence of important systemic manifestations of psoriasis including cardiovascular disorders and metabolic syndrome. About 30% of patients also develop psoriatic arthritis (PsA), which manifests as an inflammation of the synovium, entheses and spine. Therefore, the term Psoriatic Disease has been recently introduced to encompass the different clinical manifestations of this disorder.
At the skin level, psoriasis pathogenesis involves a complex interplay between T cells, dendritic cells and keratinocytes in which autoreactive CD8+ T lymphocytes have been suggested to be involved in the early phase, whereas IL-17-producing T cells play a central role in the amplification phase by enhancing the inflammatory response of keratinocytes and creating a positive feedback loop around the IL-23/IL-17 axis. A marked enhancement of IFNγ and Th1 T cell infiltration also occurs in psoriatic plaques, although the specific role of this infiltration in the pathogenesis of psoriasis is currently unclear.
Despite our progress in understanding the pathogenesis of plaque psoriasis, the immune mechanisms involved in the development of systemic disease manifestations and psoriatic arthritis remain poorly understood. As an explanation for the development of extra-cutaneous manifestations, psoriasis has been viewed as a state of systemic inflammation that progressively leads to the involvement of other organs, besides skin, via the systemic circulation. Currently, there is only limited knowledge of the soluble and cellular components that mediate this process and can lead to the development of cardiovascular manifestations and joint inflammation.
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