
In this exclusive video interview, Dr Amy Paller discusses two topics: 1) The importance of CCL17 (TARC) as a biomarker in pediatric patients with AD, and 2) How IL-4 and IL-13 contribute to skin barrier dysfunction in AD.

Dr. Simpson explores the concept of remission in AD, focusing on minimal disease activity and long-term remission, discussing how disease modification in AD can impact the course of the disease and its associated comorbidities.
Examine underlying type 2 inflammation as a driver of airway hyperresponsiveness in patients with asthma.

Dr. Ramien discusses evidence showing that advanced therapies can modify the mechanisms of atopic dermatitis, improving skin barrier function, normalizing the skin microbiome, and reducing chronic itch.

Dr. Amy Paller discusses how targeting IL-4 and IL-13 can improve burden of AD.

This video from the May 2024 ADVENT symposium at ESPD’s Annual Meeting in Košice, Slovakia features Dr. Lisa Weibel presenting how local type 2 inflammation within the skin contributes to epidermal barrier dysfunction, dysbiosis, and neuroimmune dysfunction, leading to the clinical signs and symptoms of AD. Dr. Weibel also reviews how systemic inflammation affects organ systems beyond the skin, and could potentially manifest as atopic and non-atopic comorbidities.

In this highlight video from the May 2024 ADVENT symposium at ESPD’s Annual Meeting in Košice, Slovakia, Dr. Lisa Weibel discusses how type 2 inflammation contributes to epidermal barrier dysfunction and AD signs and symptoms.

In this highlight video from the May 2024 ADVENT symposium at ESPD’s Annual Meeting in Košice, Slovakia, Dr. Lisa Weibel presents how type 2 inflammation contributes to dysbiosis, skin infections, and itch in patients with AD.

Dr. Casale discusses the critical role of barrier disruption in atopic dermatitis

Watch this short video to learn how type 2 inflammation, skin barrier dysfunction, and neurosensitization contribute to chronic itch and the itch-scratch cycle in atopic dermatitis
Examine underlying type 2 inflammation as a driver of airway hyperresponsiveness in patients with asthma.