Mihaela Surcel, Radu Huica, Carolina Constantin, Cornel Ursaciuc and Monica Neagu* Pages 3 - 11 ( 9 )
The psoriatic disease has a multi-factorial determinism being generated by a complex array of genetic, immunologic, and environmental factors. In this array, cellular interplay takes place maintaining the epidermal equilibrium. Psoriasis pathophysiology is characterized by keratinocytes hyperproliferation and immune cell infiltration in the dermis and epidermis. Innate and adaptive immune cells are highly involved, the main cellular players being dendritic and T lymphocytes, among other cells. Th17-type cytokines (e.g.,, IL-17A, IL-17F, IL-22, IL-21) as regulatory are at the core of psoriasis pathogenesis. Cytokines that emerge due to the activation of lymphocytes maintain a chronic inflammatory response acknowledged in the psoriatic skin. In vivo and in vitro cellular models, along with clinical trials that acknowledge cytokines as biomarkers and therapy targets are presented.
Autoimmunity, biomarkers, chemokines, cytokines, psoriasis, Th17.
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