Introduction
Psoriasis is a chronic, inflammatory, immune-mediated disease of the skin induced by excessive activation of adaptive immune system. Different cell types release cytokines which lead to activation of myeloid dendritic cells. Subsequently myeloid dendritic cells activate TH1, TH17 and TH22 through interleukin-12 (IL-12) and IL-23 secretion. These T helper cells eventually lead to downstream proliferation of keratinocytes, overexpression of endothelial adhesion molecules, angiogenesis and infiltrations of immunocytes to the skin which are responsible for psoriasis development. 1