Interleukin-23/Th17, Th1-Th2-Th17 and nuclear factor-κB in the pathogenesis of psoriasis

Psoriasis vulgaris is a multifactorial genetic disease.Recent advances in genetic and immunological studies have revealed that the changes in interleukin (IL)-23/T helper type 17 (Th17) cells,Th1-Th2-Th17 and nuclear factor-κB pathways are risk factors for psoriasis.The secretion of various cytokines (such as IL-17 and IL-22) involved in these pathways is increased in psoriatic lesions.Unrestrained,the activated inflammatory cytokines network in psoriasis may trigger a vicious cycle of inflammation and cellular proliferation that ultimately results in lesion formation.Deeply understanding these pathways may pave the path to tailor treatment on the basis of an individual's genetic and immunologic profile. Key words: Psoriasis;  Interleukins