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