
This infographic illustrates the clinical manifestations, pathophysiology and impact on patients of skin dyspigmentation in Prurigo Nodularis.
Learn about the role of type 2 inflammation in the burden and pathophysiology of mucus plugging in severe asthma

Join Dr. Shawn Kwatra in discussing the diverse clinical presentations of PN and the role of type 2 inflammation in disease pathogenesis.

Explore the clinical presentation and pathophysiology of chronic spontaneous urticaria in this animated video. Learn about the complex mechanism of disease involving mast cell activation and the release of inflammatory mediators.
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.
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.

Learn how loss of smell in CRSwNP is a key symptom for both patients and providers.
Learn about the significant burden that patients with COPD experience and the role of inflammatory mechanisms in this chronic, often progressive disease.
Understand the pathophysiology and clinical relevance of mucus plugs in COPD that ultimately contribute to worse outcomes for patients.
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.
Professor Sarina Elmariah describes how IL-4 and IL-13, key drivers of type 2 inflammation, uniquely contribute to manifestations of prurigo nodularis beyond itch.