ABSTRACT
Introduction
Atopic dermatitis (AD) is a common, chronic inflammatory skin disorder driven by an intricate interplay of genetic, environmental, and immunological factors.
Areas covered
As a clinically heterogenous condition, AD may be stratified into subtypes based on factors including, chronicity, immunoglobulin E levels, severity, age, and ethnicity. Transcriptomic and proteomic analyses in skin and blood help elucidate the underlying molecular mechanisms of these AD subtypes, referred to as AD endotypes. Further characterizing AD endotypes using reliable biomarkers can facilitate the development of more effective and personalized therapeutics and improve our tools for monitoring disease progression and therapeutic response across a diverse subset of patients. Here, we aim to provide perspective on the latest research regarding AD stratification using skin and blood-based studies and insight into the implications of these findings on the future of AD research and clinical practice.
Expert Opinion
The precise stratification of AD endotypes will allow for the development of reliable biomarkers and a more personalized medical treatment approach. Clinical practice and trials will eventually be able to bridge clinical with molecular data to optimize individualized treatments and more effectively monitor treatment response.
Article highlights
Atopic dermatitis (AD) is a complex, inflammatory skin condition with a heterogeneous clinical presentation.
AD is characterized as a Th2-driven disease, with variable contribution of Th1, Th17, and Th22 immune dysregulation based on patient subgroup.
Using skin and blood transcriptomic and proteomic profiling, AD has been stratified into endotypes based on various factors, including age, severity, and ethnicity.
The stratification of AD into endotypes allows for the development of a more reliable set of biomarkers to track disease progression and treatment response.
A comprehensive integration of molecular data sets will allow for a more personalized medical approach in AD and inflammatory skin diseases at large.
Declaration of interest
E Guttman-Yassky is an employee of Mount Sinai. E Guttman-Yassky has received research grants (paid to the institution) from Boehringer Ingelheim, Leo Pharma, Pfizer, Cara Therapeutics, UCB, Kyowa Kirin, RAPT, Amgen, GSK, Incyte, Sanofi, Bristol Meyers Squibb, Aslan, Regeneron, Anaptysbio, Concert, Janssen. E Guttman-Yassky is a consultant for Abbvie, Almirall, Amgen, AnaptysBio, Apogee Therapeutics, Apollo Therapeutics Limited, Artax Biopharma Inc., AstraZeneca, Bristol Meyers Squibb, Boerhinger-Ingelhiem, Cara Therapeutics, Centrexion Therapeutics Corporation, Connect Biopharm, Eli Lilly, Enveda Biosciences, Escient Pharmaceuticals, Inc., Fairmount Funds Management LLC, Forest Laboratories Galderma, Gate Bio, Google Ventures (GV), GSK Immunology, Horizon Therapeutics U.S.A., Inc., Incyte, Inmagene, Janssen Biotech, JT Central Pharmaceutical Research Institute, Jasper Therapeutics, Kyowa Kirin, Leo Pharma, Merck, Nektar Therapeutics, Novartis Pharmaceuticals Corporation, NUMAB Therapeutics AG, OrbiMed AdvisorsLLC, OTSUKA, Pfizer, Pharmaxis Ltd, Pioneering Medicine VII, Inc., Proteologix US Inc, RAPT, Regeneron Pharmaceuticals, RibonTherapeutics, Inc., Sanofi, SATO, Schrödinger, Inc., Sun Pharma Advanced Research Company (SPARC), Teva Branded Pharmaceutical Products R&D, UCB. J Krueger has acted as a consultant AbbVie, Aclaris, Allergan, Almirall, Amgen, Artax Biopharma, Arena, Aristea, Boehringer Ingelheim, Bristol-Myers Squibb, Escalier, Janssen, Kyowa Kirin, Lilly, MoonLake Immunotherapeutics, Takeda, Novartis, Nuvig Therapeutics, Target- Derm, UCB, UNION therapeutics, Valeant, Ventyx. J Krueger has received grant support (to The Rockefeller University) from AbbVie, Akros, Allergan, Amgen, Artax Bio, Avillion, Boehringer Ingelheim, Bristol-Myers Squibb, Innovaderm, Incyte, Janssen, Kyowa Kirin, Lilly, Takeda, Novartis, Provectus Pharmaceuticals, UCB, Vitae Pharmaceuticals, Xencor. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
Reviewer disclosure
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.