AI Networking Cookbook: Practical recipes for AI-assisted network automation and development
TL;DR
Current knowledge of barrier dysfunction, immune heterogeneity, molecular endotypes, molecular endotypes, microbiome imbalance, neuroimmune signaling, and mechanism-based therapies are synthesized.
Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disease driven by a combination of genetic predisposition, epidermal barrier dysfunction, immune dysregulation, aberrant neuroinflammatory signaling, and environmental factors. Genetic defects in barrier-related molecules, particularly loss-of-function mu...
BACKGROUND Atopic dermatitis (AD) is a chronic inflammatory skin disorder marked by immune dysregulation, epidermal barrier dysfunction, microbiome imbalance, pruritus, and xerosis. Despite therapeutic advances, topical treatments remain the foundation of AD management across all severities. However, most existing topi...
Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disease characterized by epidermal barrier dysfunction, immune dysregulation, microbial imbalance, and severe pruritus. Emerging evidence establishes that barrier disruption is a central pathogenic driver capable of initiating inflammatory signaling, neur...
Atopic dermatitis (AD) is a common, chronic, relapsing inflammatory skin disease characterized by xerosis, pruritus and eczematous lesions, arising from the interplay between skin barrier dysfunction and a predominantly T-helper-2 (Th2)-polarized immune response. A defining and clinically important feature of AD is its...
Atopic dermatitis (AD) is a chronic, relapsing, and remitting condition that affects approximately 10% of the population. It is a multifactorial disease involving immune dysregulation, gene mutations, and environmental factors that ultimately disrupt skin barrier restoration, causing pruritic lesions. Given the marked...
Abstract Atopic dermatitis (AD) is a chronic condition driven by epidermal barrier disruption and multiphasic immune dysregulation involving type 2, Th1, Th17, and Th22 pathways. Beyond local cutaneous pathology, systemic interactions mediated by the bidirectional gut–skin axis play an integral role, in which intestina...
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