Abstract
Atopic dermatitis (AD) is the most common inflammatory skin disease. Recent research findings have provided an insight into the complex pathogenic mechanisms involved in this disease. Despite a rising prevalence, effective and safe therapeutics for patients with moderate-to-severe AD are still lacking. Biomarkers of lesional, nonlesional skin, and blood have been developed for baseline as well as after treatment with broad and specific treatments (i.e., cyclosporine A and dupilumab). These biomarkers will help with the development of novel targeted therapeutics and assessment of disease reversal, with the promise of a more personalized treatment approach. Since AD involves more than one subtype (i.e., intrinsic/extrinsic, pediatric/adult, etc.), these molecular fingerprints needs to be validated in all subpopulations with AD.
Highlights
Atopic dermatitis (AD) causes substantial morbidity and greatly impacts quality of life of affected individuals and their families [1]
AD lesions, and further evaluation of potential similarities and differences between AD and psoriasis, have considerably enhanced our understanding of the pathogenic mechanisms of AD. While these findings indicate that AD is primarily an immune-mediated disease, we are starting to recognize that the pathogenesis of AD may be more complex than previously implied by the above two hypotheses [22,23,24]
These data may suggest that a personalized medicine approach might be possible for AD patients, with therapeutic options extending beyond targeting the Th2 pathway, to treatments targeting the Th17 and Th22 pathways, as should be clarified through future clinical trails [51]
Summary
Atopic dermatitis (AD) causes substantial morbidity and greatly impacts quality of life of affected individuals and their families [1]. AD lesions, and further evaluation of potential similarities and differences between AD and psoriasis, have considerably enhanced our understanding of the pathogenic mechanisms of AD While these findings indicate that AD is primarily an immune-mediated disease, we are starting to recognize that the pathogenesis of AD may be more complex than previously implied by the above two hypotheses [22,23,24]. An important breakthrough in the understanding of disease pathogenesis was provided by studies investigating genomic and histologic profiling of AD skin [39,40] These studies have defined sets of biomarkers of the lesional AD skin, which are correlated with disease activity [39,40]. With the exception of IL-31, CCL17, ECP, eosinophils, and IgE, none of these serum biomarkers have been shown to be treatment response biomarkers [45,46,47]
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