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Link to original content: http://pubmed.ncbi.nlm.nih.gov/36928371/
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Review
. 2023 May;20(5):448-474.
doi: 10.1038/s41423-023-00992-4. Epub 2023 Mar 16.

The translational revolution in atopic dermatitis: the paradigm shift from pathogenesis to treatment

Paola Facheris  1   2 , Jane Jeffery  3 , Ester Del Duca  1 , Emma Guttman-Yassky  4   5
Affiliations
Review

The translational revolution in atopic dermatitis: the paradigm shift from pathogenesis to treatment

Paola Facheris et al. Cell Mol Immunol. 2023 May.

Abstract

Atopic dermatitis (AD) is the most common inflammatory skin disease, and it is considered a complex and heterogeneous condition. Different phenotypes of AD, defined according to the patient age at onset, race, and ethnic background; disease duration; and other disease characteristics, have been recently described, underlying the need for a personalized treatment approach. Recent advancements in understanding AD pathogenesis resulted in a real translational revolution and led to the exponential expansion of the therapeutic pipeline. The study of biomarkers in clinical studies of emerging treatments is helping clarify the role of each cytokine and immune pathway in AD and will allow addressing the unique immune fingerprints of each AD subset. Personalized medicine will be the ultimate goal of this targeted translational research. In this review, we discuss the changes in the concepts of both the pathogenesis of and treatment approach to AD, highlight the scientific rationale behind each targeted treatment and report the most recent clinical efficacy data.

Keywords: Atopic dermatitis; biomarkers; eczema; translational revolution.

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Conflict of interest statement

EGY is an employee of Mount Sinai and has received research funds (grants paid to the institution) from AbbVie, Almirall, AnaptysBio, Boehringer-Ingelheim, Celgene, Dermavant, DS Biopharma, Eli Lilly, Innovaderm, Janssen, Kiniska, KyowaKirin, Novan, Pfizer, Regeneron, Ralexar, Glenmark, Galderma, Asana, Innovaderm, Leo Pharma, Sienna Biopharm, Union Therapeutics, and UCB. EGY is also a consultant for Sanofi Aventis, Regeneron, Cara Therapeutics, Celgene, Concert, Amgen, Boehringer-Ingelheim, DBV, Dermira, DS Biopharma, EMD Serono, Escalier, Flx Bio, Galderma, Glenmark, Incyte, Kyowa Kirin, Novartis, Pfizer, Leo Pharma, AbbVie, Eli Lilly, Kyowa, Mitsubishi Tanabe, Asana Biosciences, Sienna Biopharm, and Union Therapeutics. The rest of the authors declare no competing interests.

Figures

Fig. 1
Fig. 1
Schematic representation of the immune markers involved in the pathogenesis of AD and systemic drugs approved or that have been in clinical trial development for AD. In red boxes are reported molecules currently under investigation or with positive results in clinical trials, and in blue boxes are reported drugs that failed to reach primary endpoints in clinical trials. CRTH2 prostaglandin D2 receptor 2, DC dendritic cell, DRG dorsal root ganglion, H4R histamine H4 receptor, IL interleukin, KOR kappa opioid receptor, NK1R neurokinin1, OSM oncostatin M, OSMRB oncostatin M specific receptor subunit beta, OX40 tumor necrosis factor receptor superfamily, member 4, OX40L OX40 ligand, TSLP thymic stromal lymphoprotein, TRPA1 transient receptor potential cation channel, subfamily A, member 1, TRPV1 transient receptor potential vanilloid-1
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