The role of calreticulin in etiopathogenesis of psoriasis

Psoriasis is a common chronic inflammatory disease of skin with remissions and relapses. This disease, which can affect skin, nails and joints, is characterized by erythematous, pearly thick scale, sharp limited plaques, although there are clinically different forms. Etiopathogenesis is thought to be a multigenetic and multifactorial disease, although many studies have not yet been clarified. The main pathological changes are keratinocyte hyperproliferation, inflammation and vascular changes. Psoriasis is known to be a T-cell mediated inflammatory disease, but the factors that influence this initiation and maintenance of inflammation in the psoriatic skin have not yet been clarified. It is not yet known in psoriasis whether healthy keratinocytes proliferate secondary to inappropriate T cell response, or an abnormality in keratinocytes trigger the inflammation. This hyperproliferative keratinocytes have been shown to incomplete differentiation and decreased keratinocyte apoptosis. Calreticulin is a multifunctional endoplasmic reticulum chaperone protein. In addition to controlling protein folding, one of its most important functions is the provision of intracellular calcium hemostasis. It is also involved in the inhibition of angiogenesis in cell adhesion and migration, recognition of apoptotic cells at the cell surface, triggered by apoptosis. It may be thought that calreticulin, which has not previously been studied in psoriasis as far as we know, may play a role in the pathogenesis of psoriasis by pathological pathways such as apoptosis resistance, induction and maintenance of inflammation as a result of clearing apoptotic cells, and reduction of angiogenesis inhibition.