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Date publication
octobre 2022
Journal
Clinical and translational medicine
Auteurs
Membres identifiés du Cancéropôle Est :
Pr JOUZEAU Jean-Yves
Tous les auteurs :
Gautam P, Maenner S, Cailotto F, Reboul P, Labialle S, Jouzeau JY, Bourgaud F, Moulin D
Lien Pubmed
Résumé
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 (IκBζ) is an atypical transcriptional factor of the IκB protein family since, contrary to the other family members, it positively regulates NF-κB pathway by being exclusively localized into the nucleus. IκBζ deficiency reduces visible manifestations of experimental psoriasis by diminishing expression of psoriasis-associated genes. It is thus tempting to consider IκBζ 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 IκBζ, its downstream targets, its involvement in pathogenesis of multiple disorders with emphasis on psoriasis and evidences supporting that inhibition of IκBζ may be a promising alternative to current therapeutic managements of psoriasis.
Mots clés
NFKBIZ, ikappabZeta, IκBζ, inflammation, psoriasis
Référence
Clin Transl Med. 2022 10;12(10):e1032
