Author contributions: P.-J.H. participated in the data collection and coordination and analyzed the clinical data. L.-E.Y. participated in the data collection. W.-M.K. and Z.-G. Q. conceived the study, participated in its design and coordination, and analyzed the clinical data. All authors helped draft the manuscript. Patient consent: Written consent for publication was obtained from the patients.

Skin epidermis constitutes the outer permeability barrier that protects the body from dehydration, heat loss, and myriad external assaults. Mechanisms that maintain barrier integrity in constantly challenged adult skin and how epidermal dysregulation shapes the local immune microenvironment and whole‐body metabolism remain poorly understood. Here, we demonstrate that inducible and simultaneous ablation of transcription factor‐encoding Ovol1 and Ovol2 in adult epidermis results in barrier dysregulation through impacting epithelial‐mesenchymal plasticity and inflammatory gene expression. We find that aberrant skin immune activation then ensues, featuring Langerhans cell mobilization and T cell responses, and leading to elevated levels of secreted inflammatory factors in circulation. Finally, we identify failure to gain body weight and accumulate body fat as long‐term consequences of epidermal‐specific Ovol1/2 loss and show that these global metabolic changes along with the skin barrier/immune defects are partially rescued by immunosuppressant dexamethasone. Collectively, our study reveals key regulators of adult barrier maintenance and suggests a causal connection between epidermal dysregulation and whole‐body metabolism that is in part mediated through aberrant immune activation.

Dengue virus (DENV) is a single-stranded RNA virus that is transmitted by Aedes aegypti and Aedes albopictus. As a global health problem, early diagnosis and timely treatment of DENV are imperative. Therefore, it is important to explore the association between dengue fever and hepatitis and its pathogenesis and development mechanism of action. This may lead to the identification of biological markers for the prevention and treatment of dengue fever-induced hepatitis. In this study, we identified differentially expressed genes associated with interferon signaling to further understand the relationship between dengue fever and hepatitis. It has been speculated that during dengue-induced hepatitis, DEXD/H-box helicase 58 (DDX58) and interferon-induced protein with tetratricopeptide repeats 1 (IFIT1) are primarily responsible for pathogen identification. The joint action of HECT and RLD domain containing E3 ubiquitin protein ligase 5 (HERC5) and ubiquitinspecific peptidase 18 (USP18) regulate the biological effects of interferon and participate in the occurrence and development of this disease.

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