Immune modules to guide diagnosis and personalized treatment of inflammatory skin diseases.

Previous advances have identified immune pathways associated with inflammatory skin diseases, leading to the development of targeted therapies. However, there is a lack of molecular approaches that delineate these pathways at the individual patient level for personalized diagnostic and therapeutic guidance. Here, we conduct a cross-comparison of expression profiles from multiple inflammatory skin diseases to identify gene modules defining relevant immune pathways.

From Viral Infection to Skin Affliction: Unveiling Mechanisms of Cutaneous Manifestations in COVID-19 and Post-COVID Conditions.

COVID-19 skin manifestations are multifaceted, ranging from urticaria, morbilliform or papulovesicular rash, livedoid purpuric lesions, and to pseudochilblains (also called COVID toes). Recent insights into the mechanism of these manifestations have highlighted that morbilliform, papulovesicular, and livedoid/purpuric rashes are related to virus-induced endothelial cell damage and linked to moderate-to-severe disease, whereas pseudochilblains are related to an exaggerated IFN-1 production by plasmacytoid dendritic cells in protected individuals. In this paper, we will review the clinical and physiopathological features of cutaneous COVID-19 manifestations in relation to the direct viral cytopathic effects and dysregulated IFN-1 responses.

IL-9 sensitizes human T2 cells to proinflammatory IL-18 signals in atopic dermatitis.

Background: T2 cells crucially contribute to the pathogenesis of atopic dermatitis (AD) by secreting high levels of IL-13 and IL-22. Yet the upstream regulators that activate T2 cells in AD skin remain unclear. IL-18 is a putative upstream regulator of T2 cells because it is implicated in AD pathogenesis and has the capacity to activate T cells.