| Abstract: | Atopic dermatitis (AD) and psoriasis are common chronic and relapsing inflammatory skin diseases mainly mediated by T cells. Type 2 and 17 inflammations are essential in the pathogenesis of AD and psoriasis, respectively. Clinical evidence suggests that benvitimod, a natural metabolite produced by bacterial symbionts, plays a therapeutic role in the development and progression of both AD and psoriasis. Mechanistically, the two most potent interactions with benvitimod are observed in the aryl hydrocarbon receptor (AhR) and nuclear factor-erythroid 2-related factor-2 (Nrf2) pathways. However, it remains largely unknown how is the local interplay among benvitimod, AhR, and Nrf2, and how the epithelial microenvironment contributes to the complex inflammatory context that results in the treatment of AD and psoriasis. In the present study, the modulatory effects of benvitimod on treating AD and psoriasis. |
