The IL-4, IL-13 and IL-31 pathways in atopic dermatitis

ABSTRACT

Introduction: Atopic dermatitis (AD) is the most common inflammatory skin disease. It has a complex pathophysiology, with a combination of immune dysregulation and intrinsic barrier defects driving cutaneous inflammation and allergic symptomatology. The IL-4, IL-13 and IL-31 inflammatory pathways have been identified as hallmark features in the pathogenesis of the disease, contributing uniquely and synergistically to immune and barrier abnormalities as well as the key symptoms, such as pruritis. Novel therapeutics that target these pathways have been under development to find treatments for AD.

Areas covered: This review discusses the IL-4, IL-13 and IL-31 pathways in AD. We will also detail novel targeted therapeutics that have recently been or are currently in clinical trials for AD. A literature search was conducted by querying Scopus, Google Scholar, PubMed, and Clinicaltrials.gov up to January 2021 using combinations of the search terms ‘IL-4’ ‘IL-13’ ‘IL-31’ ‘atopic dermatitis’ ‘immune pathway’ ‘biologics’ ‘novel therapeutics’ ‘JAK/STAT inhibitors.’

Expert opinion: The complex pathophysiology of AD advocates for innovation. Novel minimally invasive sampling modalities such as tape stripping will allow for a broader characterization of the immunomechanisms behind AD pathophysiology. This will allow for the continued development of a personalized medicine approach to treat AD.

KEYWORDS:

• Atopic dermatitis
• biologics
• dupilumab
• interleukin-4
• interleukin-13
• interleukin-31
• jak-inhibitors
• th2
• therapeutics

Declaration of interest

Emma Guttman-Yassky is an employee of Mount Sinai and has received research funds (grants paid to the institution) from Abbvie, Amgen, AnaptysBio, AstraZeneca, Boerhinger-Ingelhiem, Cara Therapeutics, Innovaderm, Janssen, KAO, Kyowa Kirin, Leo Pharma, Pfizer, Regeneron Pharmaceuticals, Inc. and UCB; and is a consultant for Abbvie, Almirall, Amgen, Arena, Asana Biosciences, AstraZeneca, Boerhinger-Ingelhiem, Bristol-Meyers Squibb, Cara Therapeutics, Connect Pharma, Eli Lilly, EMD Serono, Evidera, Galderma, Ichnos Sciences, Incyte, Janssen Biotech, Kyowa Kirin, Leo Pharma, Pandion Therapeutics, Pfizer, Ribon, RAPT Therapeutics, Regeneron Pharmaceuticals, Inc., Sanofi, SATO Pharmaceutical, Siolta Therapeutics, Target PharmaSolutions, UCB and Ventyx Biosciences. The authors have no 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.

Reviewers disclosure

Peer reviewers on this manuscript have no relevant financial relationships or otherwise to disclose.

Additional information

Funding

This paper was not funded.