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New Trends in the Immunopathogenesis of Psoriasis

Psoriasis is a chronic hyperproliferative inflammatory skin disease characterized by abnormal keratinocyte hyperproliferation and differentiation, intra-epidermal accumulation of neutrophil granulocytes, and dermal inflammatory infiltrate that mostly consists of T-cells. Today, psoriasis is definitely recognized as a T-cell-mediated inflammatory disease. Infiltration of T-cells seems to be the primary event that precedes the keratinocyte hyperproliferation. It is suggested that systemic lymphocity activation is followed by the activation of intradermal CD8+ T-cells. So far, it seems that CD4+ T-cells create an appropriate type-1 cytokine environment for CD8 T-cells activation that eventually trigger the psoriatic cascade. Thus, T-cells are responsible for initiation and maintenance of psoriasis.However, it seems that the specific immune reaction to a putative antigen, mediated by T-cells leads to creation of psoriatic lesions. The immune reaction constantly driven by bacterial superantigens or epidermal self-antigens eventually leads to development of psoriatic lesions. The psoriatic process is a dynamic process that includes interaction between Th1- and Tc1-cells as well as between T-cells and keratinocytes. The better understanding of the immunopathogenesis of psoriasis would allow for development of specific T-cell-targeted and/or cytokine-targeted new therapies.

(cytokines; immunopathogenesis; keratinocytes; T lymphocytes)

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