
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

In this highlight video from the September 2024 ADVENT symposium at EADV’s Annual Meeting in Amsterdam, the Netherlands, Dr. Stephan Weidinger discusses how type 2 inflammation contributes to epidermal barrier dysfunction, perivascular infiltration and plasma protein leakage, and chronic itch in AD.
In this soundbite video from the April 2025 ADVENT Forum in Lisbon, Portugal, Dr. Eric Simpson outlines why early, targeted control of type 2 inflammation may modify the course of atopic dermatitis by addressing upstream drivers of barrier dysfunction, dysbiosis, and itch.

In this soundbite video from the April 2025 ADVENT Forum in Lisbon, Portugal, Dr. Brian Kim explains how underlying type 2 inflammation sustains the chronic itch-scratch cycle in atopic dermatitis, highlighting the interplay of barrier dysfunction, cytokine signaling, and neuronal activation.
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.

In this soundbite video from the April 2025 ADVENT Forum in Lisbon, Portugal, Prof. Oscar Palomares explains how type 2 inflammation and barrier dysfunction contribute to the development of atopic comorbidities and increased susceptibility to infections.

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.