Therapeutic Potential of Rlip Loss on Atopic Dermatitis

Abstract

Rlip knockdown protects p53 deficient mice from carcinogenesis and reduces inflammation. In Rlip null mice, increased oxidative stress alone was not enough to increase inflammation. Thus, Rlip is necessary to translate oxidative stress into inflammation. Rlip knockdown disrupts inflammatory signaling in atopic dermatitis through altering Th1/Th2 immune genes. Here we review potentially significant genes by analysis of RNA sequence pathways in a previously unknown role, atopic dermatitis, in relation to partial Rlip loss.