Kastelan Marija, Massari Larisa Prpić, Pasić Aida, Gruber Franjor
Department of Dermatovenerology, Rijeka University Hospital Center, Kresimirova 42, 51000 Rijeka, Croatia.
Acta Dermatovenerol Croat. 2004;12(1):26-9.
Psoriasis is a chronic hypeproliferative 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 lymphocyte activation is followed by the local accumulation of specific CD4+ T-cells and subsequently 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. The precise mechanism how activated T-cells trigger psoriasis is yet unknown. 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.
