134 search results for: Pathophysiology
Skin Dyspigmentation In Prurigo Nodularis (PN)
This infographic illustrates the clinical manifestations, pathophysiology and impact on patients of skin dyspigmentation in Prurigo Nodularis.
Type 2 Inflammation Underpins Pediatric Severe Asthma
Learn about the role type 2 inflammation plays in the burden and pathophysiology of severe asthma in pediatric patients.
Type 2 Inflammation Mediates Severe Asthma in Pediatric Patients
Dr. Leonard Bacharier discusses how type 2 inflammation underlies the pathophysiology of pediatric severe asthma and contributes to burden.
ERS 2024 | Airway Remodeling: A Permanent or Transitory Consequence in Severe Asthma Patients?
Professors Celeste Porsbjerg and Klaus Rabe and Dr Mario Castro discuss the pathophysiology of airway remodeling and its impact on patients with severe asthma.
Type 2 Inflammation in AD Manifestations in Skin and Body
Dr. Ramien discusses the role of type 2 inflammation in the pathophysiology of atopic dermatitis, and highlights the association of atopic dermatitis with systemic diseases and comorbidities.
The Path to Nodules: Type 2 Inflammation at the Core of Chronic Itch and Fibrosis in Prurigo Nodularis
Join Dr. Shawn Kwatra in discussing the diverse clinical presentations of PN and the role of type 2 inflammation in disease pathogenesis.
ADVENT On Air | Charting a New Course: The Frontier of Early Intervention and Disease Modification in AD
Join Drs. April Armstrong and Lisa Beck for a conversation around the long-term burden and effects of AD. They will discuss the underlying pathophysiology of AD and how early intervention and disease modification may impact disease course.
How Does Protective Type 2 Immunity Become Harmful Type 2 Inflammation?
In this video from the March 2025 ADVENT symposium in Orlando, Florida, Dr. Eric Simpson discusses how protective type 2 immunity can become dysregulated, leading to harmful type 2 inflammation. The associated inflammatory process can contribute to the pathophysiology of several dermatological diseases, including AD, PN, CSU, and BP.
On the Surface: Restoring the Skin Barrier in Patients With AD
In this video from the April 2025 WCPD symposium, Dr Amy Paller discusses the pathophysiology of skin barrier dysfunction in AD and how regulating IL-4 and IL-13 signaling may lead to restoration of the skin barrier. Dr Paller goes on to explore how reducing certain biomarkers, such as CCL17 (TARC), may reduce inflammation that contributes to AD severity in pediatric patients.
The Benefits of Early Intervention in Reducing the Burden of Disease in Children With Atopic Dermatitis
This page presents educational material, infographics, and video highlights from our recent ADVENT symposia, including the 2025 World Congress of Pediatric Dermatology (WCPD) in Buenos Aires, Argentina, exploring the pathophysiology of type 2 inflammation and atopic dermatitis, the burden of disease leading to cumulative life course impairment (CLCI), and the risk of the atopic march in pediatric patients with atopic dermatitis.
The Role of IL-4 and IL-13 in CSU Pathogenesis
Dive into the complex pathophysiology of chronic spontaneous urticaria (CSU), where mast cell degranulation drives the hallmark signs and symptoms. This interactive infographic elucidates how key type 2 cytokines, specifically IL-4 and IL-13, contribute to mast cell activation, immune cell trafficking into the skin, and neuronal sensitization in CSU, which ultimately leads to the release of mediators like histamine that cause wheals, angioedema, and itch.
What Went Wrong? How Dysregulated Type 2 Immunity Contributes to AD, PN, CSU, and BP
The March 2025 ADVENT symposium in Orlando, Florida brought together 4 dermatology experts to explore the evolving science of type 2 inflammation. Type 2 inflammation plays a central role in the pathophysiology of multiple dermatological diseases, driving chronic immune dysregulation that affects patients with atopic dermatitis (AD) prurigo nodularis (PN), chronic spontaneous urticaria (CSU) and bullous pemphigoid (BP). Understanding the mechanisms behind type 2 inflammation is key to advancing care and improving patient quality of life.
