Type 2 inflammation contributes to many dermatologic diseases, which may lead to potentially life-changing burdens and challenges to patients and caregivers. By uncovering the role of type 2 inflammation in the pathophysiology of AD, PN, CSU, and BP, we can move forward in our understanding of each disease. Join global experts for an educational symposium on March 8th that will uncover the role of type 2 inflammation in the pathophysiology of AD, PN, CSU, and BP and explore questions driving current research in each disease.
The underlying pathophysiology of atopic dermatitis (AD) is driven by dysregulation of type 2 immunity that contributes to skin barrier dysfunction. AD typically develops very early in life and children with AD often develop other atopic conditions such as food allergy, asthma, and allergic rhinitis in a progression called the atopic march. Early treatment may help reduce the atopic march and other comorbidities to lessen the lifetime burden created by these diseases. There may even be a window of opportunity for disease modification.

Professor Lisa Beck explores the chronic and persistent burden of atopic dermatitis (AD) as well as the concept of early intervention in patients with AD.

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.

In this highlight video from the October 2024 ADVENT symposium at EAPS in Vienna, Austria, Dr Christine Bangert discusses how type 2 inflammation contributes to epidermal barrier dysfunction and chronic itch in AD