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Atopic dermatitis (AD) is an inflammatory dermatosis with a pathogenesis believed to be due to a combination of genetic, immunologic and environmental factors that affects up to 5% of adults and 20% of children worldwide. 1,2 Common genetic factors include polymorphisms in the filaggrin structural protein, interleukin (IL)-4 receptor and vitamin D receptor. [3][4][5] AD is driven by multiple immune pathways, most commonly with activation of Th2 and Th22 T-cell subsets. 6 Crosstalk between commensals and the host immune system modulates adaptive and innate immune responses in AD. 7 Staphylococcus aureus (SA) in AD lesions and surrounding normal skin was first noted by Leyden et al. in the 1970s; since then, the understanding of its role in AD has drastically evolved. 8,9 SA is a well-established exacerbator of AD; it is frequently isolated from the skin of AD patients and increased SA density is found during flares. 10 A meta-analysis in 2016 reported a pooled prevalence of SA colonization among AD patients of 70% in lesional skin, 39% in non-lesional skin and 62% in the nose. 11 More recently, Kong et al 12 found that AD treatments and flares were closely associated with shifts in the cutaneous microbial diversity. While current evidence has established that SA proliferates during flares and plays a role in the cycle of epidermal breakdown and inflammation, a true causal relationship has not been established. Herein, we will summarize the

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Aryl hydrocarbon receptor (AHR)/nuclear factor‐erythroid 2‐related factor 2 (NRF2) modulation is emerging as novel targets in the treatment of atopic dermatitis and other inflammatory skin disorders. Agonist activation of this pathway has downstream effects on epidermal barrier function, immunomodulation, oxidative stress reduction and cutaneous microbiome modulation. Tapinarof, a dual agonist of the AHR/NRF2 signalling pathway, has shown promise in phase 2 trials for atopic dermatitis. In this review, we summarize current knowledge of the AHR/NRF2 pathway and implications in skin disease process. We also review the therapeutic potential of current AHR agonists and propose future directions to address knowledge gaps.

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