Atopic dermatitis (AD) is a common chronic inflammatory skin disease that often begins in childhood but may persist into or arise in adulthood, affecting millions of people worldwide. Major advances have clarified key aspects of its pathophysiology, including type 2 immune responses, epithelial barrier dysfunction, neuroimmune signaling, and alterations in the skin microbiome. However, important questions remain, particularly regarding the mechanisms that drive disease heterogeneity, long-term persistence, and the transition from intermittent flares to chronic immune dysregulation.

AD also shares overlapping inflammatory pathways with several immune-mediated disorders, including allergic, respiratory, lupus (SLE), arthritic (RA), and ophthalmologic conditions. These comorbidities may reflect interconnected pathogenic mechanisms involving IgE-associated responses and broader type 2 immune dysregulation that sustain inflammation across multiple tissues. A deeper understanding of these shared and distinct pathways is essential for identifying biomarkers, refining disease classification, and supporting the development of more precise and effective therapies.

This Research Topic aims to bring together high-quality, up-to-date research that advances our understanding of the inflammatory mechanisms underlying AD and related immune-mediated disorders. By integrating basic, translational, and clinical studies, we seek to define key cellular and molecular pathways, identify shared and disease-specific mechanisms, and highlight novel biomarkers and emerging therapeutic targets.

We particularly welcome rigorous and innovative contributions that clarify the drivers of disease heterogeneity, identify predictors of disease progression or treatment response, and expand mechanistic insight into both cutaneous and systemic inflammation. Our goal is to accelerate the translation of scientific discoveries into more precise, targeted, and effective therapeutic strategies that improve long-term patient outcomes.

We invite submissions that provide novel insights into the mechanistic, translational, and early clinical aspects of the inflammatory pathways underlying AD and related immune-mediated diseases. We welcome contributions from fundamental immunology, translational research, and clinical investigation, particularly studies that are scientifically rigorous, conceptually clear, and clinically relevant.

Topics of interest include, but are not limited to:

- Innate and adaptive immune mechanisms in AD and related conditions, including Th2, Th22, and Th17 pathways, cytokine signaling networks, innate lymphoid cells, and inflammasome activation
- Keratinocyte and fibroblast dysfunction, barrier biology, and epithelial-immune crosstalk
- Neuroimmune mechanisms underlying itch, pain, and inflammatory signaling
- Interactions among the skin, gut microbiome, and immune system in AD and related diseases
- Genetic and epigenetic factors influencing inflammatory responses
- Biomarkers, disease endotypes, and predictors of treatment response
- Related co-morbid diseases as SLE and RA and its influence on skin barrier disruption and skin symptoms.
- Coexistence of atopic dermatitis (AD) and systemic lupus erythematosus (SLE) or rheumatoid arthritis (RA)
- Pathogenic mechanisms linking atopic dermatitis AD to other autoimmune disorders (SLE, RA, celiac disease, colitis, gut-inflammation, etc)
- Early translational and mechanistic studies of emerging therapies, including biologics, small-molecule inhibitors, monoclonal antibodies, and novel immunomodulatory strategies

We welcome original research articles, reviews, perspectives, case reports, and brief research reports that provide novel insights and advance understanding of the inflammatory mechanisms driving AD and related conditions.

Are you interested in contributing a manuscript to this Research Topic?

Inflammatory mechanisms of atopic dermatitis and related immune-mediated diseases