Psoriasis: A Disease of Systemic Inflammation with Comorbidities

The majority of the current data about psoriasis is about immune system elements and role of inflammation in the pathogenesis. The development of psoriasis is associated with genetic predisposition which has a basis of T cell activation secondary to dermal inflammation with abnormal keratinocyte proliferation. Tumor necrosis factor alpha (TNF-α), interferon gama (IFN-γ), and interleukin (IL)-8 which are secreted by T lymphocytes, keratinocytes and in‐ flammatory cells polarize type 1 T lymphocytic pathway and lead to the migration of poly‐ morphonuclear leukocytes to the epidermis predominantly [2]. Upregulation of HLADR, intercellular adhesion molecule-1 and E-selectin activates CD2+, CD3+, CD5+, CLA+, CD45RO, HLA-DR, CD25 (IL-2 receptor) and CD27 expressing T cells [2]. Migration and ac‐ cumulation of inflammatory cells in the epidermis destroyes the basal membrane and des‐ mosomes. In response to the damage, mitogenic cyokines are secreted and a similar process to wound healing results in rapid cell cycling and rapid maturation of keratinocytes [1, 2, 3].The constant inflammatory cell chemotaxis and cytokine release causes the chronic clini‐ cal course with recurrent lesions.