Genome organizer Satb1 is regulated by p63 and contributes to epidermal morphogenesis by remodeling chromatin structure and gene expression at the epidermal differentiation complex locus.

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Mast cells (MCs) are well known as versatile effector cells in allergic reactions and several other immune responses. Skin MCs and cutaneous MC responses are subject to the effects of environmental factors including ultraviolet radiation (UVR). Numerous studies have assessed the effects of UVR on MCs, in vitro and in vivo. Interestingly, UVR seems to have variable effects on non-activated and activated mast cells. In general, UV therapy is beneficial in the treatment of urticaria and mastocytosis, but the effects are variable depending on treatment regimen and type of UVR. Here, we review and summarise key reports from the older and current literature on the crosstalk of UVR and skin MCs. Specifically, we present the literature and discuss published reports on the effects of UVR on skin MCs in rodents and humans. In addition, we review the role of MCs in UVR-driven skin diseases and the influence of UV light on MC-mediated skin diseases. This summary of our current understanding of the interplay of skin MCs and UVR may help to improve the management of patients with urticaria and other MC disorders, to identify current gaps of knowledge, and to guide further research. K E Y W O R D Scancer, mast cell, ultraviolet radiation, urticaria

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Atopic dermatitis (AD) is the most common inflammatory disease of the skin characterized by defects in keratinocyte differentiation and skin barrier dysfunction. Despite its prevalence, an in vitro,commercial model of AD is not currently available to facilitate basic research and therapeutic development. Using the reconstructed full thickness human epidermal model (EpiDermFT), an inflammatory cocktail comprised of Th2 cytokines was used to induce changes to mimic an atopic dermatitis phenotype. Following treatment with IL-4, IL-13 and IL-31, significant changes in several markers of differentiation and skin barrier integrity were observed, closely resembling AD skin. Histological analysis revealed treatment with IL-4, IL-13, and IL-31 reduced the presence of the stratum granulosum and induced spongiosis in the epidermis. Upregulation of pro-inflammatory mediators, such as IL-8, and down regulation of differentiation markers (keratin 1, keratin 10, involucrin, filaggrin) were observed at both the gene and protein level. These findings demonstrate that treatment of the EpiDermFT tissue model with Th2 cytokines induces a phenotype that is consistent with the hallmarks of AD, including altered differentiation and barrier function. We anticipate that the model described here will be useful for screening and evaluating active ingredients and other molecules used in the treatment of atopic dermatitis. LB1588 Ultraviolet light-induced gasdermin c expression is mediated via trpv1/ calcium/calcineurin/nfatc1 pathway