Therapeutic Potential of Rlip Loss on Atopic Dermatitis: A Systematic Review

Abstract

Abstract Atopic dermatitis (AD) is a chronic relapsing inflammatory skin disease and is marked by dry skin and itchy papules that can become excoriated. AD can be caused by the interaction of host factors such as genetic susceptibility, immunologic responses, and skin barrier. The inflammatory environment of AD is characterized by Th2 and skin barrier dysfunction. Reactive oxygen species (ROS) are also responsible for inflammation associated with AD and the pathogenic disease process. Rlip knockdown is found to protect p53 deficient mice from carcinogenesis as well as reduce inflammation. Rlip knockdown also alters various canonical pathways and, in AD, can lead to inflammatory signaling by altering the balance of Th1 and Th2 immune genes involved in the pathogenesis of eczema. Here we suggest upregulation of ALDH3A1, ACVR1C, and IL-13RA2 through Rlip inhibition could serve as a therapeutic target for the treatment of AD through reduction of skin inflammation and maintenance of skin barrier, decreased Th2 immune response, and lowered intracellular calcium signaling involved in skin pain threshold.