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Atopic dermatitis field is undergoing a translational revolution lately with active development of novel topical and systemic
therapeutics. In psoriasis a system biology approach was instrumental in defining biomarkers of disease and therapeutic
response as well as predictors of successful response to treatment. We have lately defined a unified atopic dermatitis phenotype using
a meta-analysis approach that highlighted key features and biomarkers of atopic dermatitis. This meta-analysis derived transcriptome
(MADAD) identified wide lipid abnormalities and for the first time in vivo, correlated Th2 immune activation with down-regulation
of key epidermal lipids, emphasizing the role of cytokines on the barrier disruption in AD. MADAD is now applied to evaluate
changes with different investigational treatments, allowing us to evaluate drug effect at the transcriptomic level not only on the AD
phenotype but also the effect on suppressing specific pathways. Since many aspects of atopic dermatitis are constantly evaluated in
various mouse models, we also seek to see how well the commonly used mouse models of atopic dermatitis compare with the human
MADAD AD phenotype at the transcriptomic level and which mouse model if any captures the hallmark pathways of AD better.