**3.4 The contractile keratinocyte**

Psoriasis is associated with high levels of IFN-γ in epidermis [91]. IFN-γ strongly and specifically induced the promoter of the K17 (abnormal marker) gene. K17 is exceptional because it is not found in healthy interfollicular epidermis, but it is expressed in certain pathologic states, psoriasis [28]. The function of K17 in epidermis therefore may be to promote or allow KC contractility and/or frequent changes in shape [95]. Indeed, expression of K17 has been used to evaluate the course of treatment of psoriatic patients [63]. Due to failure, to resolve the deregulated inflammatory response in psoriasis leads to the persistent activation of KCs, which is characterized by prolonged K17 expression [13].

### **3.5 Back to normal basal phenotype**

To revert to the basal cell phenotype, KCs need a signal. This signal comes from the dermal fibroblasts in the form of TGF-β. Cell kinetics study by Van Ruissen et al. *Immunomodulatory Effect of Methotrexate Abruptly Controls Keratinocyte Activation in Psoriasis DOI: http://dx.doi.org/10.5772/intechopen.102811*

[96] clearly indicate that the TGF-β donot control KCs normal proliferation, but it controls the abnormal proliferation of KCs (antihyperproliferative). Whereas in psoriasis, the expression of TGF-β is low [97]. So the activation cycle is not reverted to normal basal phenotype, therefore hyperproliferation of KC takes place in psoriasis.
