Emerging role of I kappa B zeta inflammation: Emphasis on psoriasis

Psoriasis is a chronic inflammatory disorder affecting skin and joints that results from immunological dysfunction such as enhanced IL-23 induced Th-17 differentiation. IkappaB-Zeta (I kappa B zeta) is an atypical transcriptional factor of the I kappa B protein family since, contrary to the other family members, it positively regulates NF-kappa B pathway by being exclusively localized into the nucleus. I kappa B zeta deficiency reduces visible manifestations of experimental psoriasis by diminishing expression of psoriasis-associated genes. It is thus tempting to consider I kappa B zeta as a potential therapeutic target for psoriasis as well as for other IL23/IL17-mediated inflammatory diseases. In this review, we will discuss the regulation of expression of NFKBIZ and its protein I kappa B zeta, its downstream targets, its involvement in pathogenesis of multiple disorders with emphasis on psoriasis and evidences supporting that inhibition of I kappa B zeta may be a promising alternative to current therapeutic managements of psoriasis.