Explore how type 2 inflammation drives sinonasal barrier dysfunction in chronic rhinosinusitis with nasal polyps (CRSwNP) with this video on the cellular mechanisms behind hallmark symptoms — including nasal congestion and loss of smell.

Embark on this interactive triathlon challenge to uncover the interplay of type 2 inflammation, barrier dysfunction, and neuroimmune dysregulation in the disease pathology of CRSwNP.

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
See how type 2 inflammation underlies remodeling processes in asthma.
Explore the concept of disease modification in atopic dermatitis through this interactive infographic, which highlights potential considerations such as optimal sustained disease control, subclinical inflammation, the pathophysiology of AD, and atopic/non-atopic comorbidities.
Learn about the significant burden that patients with COPD experience and the role of inflammatory mechanisms in this chronic, often progressive disease.

Prof. Claus Bachert describes how type 2 inflammation drives CRSwNP.
Dr. Lawrence Eichenfield describes the pathophysiology of atopic dermatitis and how type 2 inflammation may sensitize patients to atopic comorbidities.

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 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.
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 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.