
This infographic highlights how PN is driven by type 2 inflammation, linking immune dysregulation, fibroblast activation, and neuronal dysfunction to nodule formation. It also shows how cytokine-mediated changes in neuronal architecture increase excitability and chronic itch, where resulting lesions and scarring significantly impact patients’ psychological well-being.

Dr. Palomares discusses how type 2 inflammation, an aberrant immune response, underlies skin diseases like atopic dermatitis, prurigo nodularis, and chronic spontaneous urticaria, linking to their clinical symptoms.

Join Professor Hide as he describes the potential role of Type 2 inflammation in the pathogenesis of CSU.

Join Dr. Brian Kim in discussing the diagnosis of CPUO and the role of type 2 inflammation in disease pathophysiology.
Professor Matthias Augustin highlights the role of type 2 inflammation in chronic itch across distinct pruritic skin diseases and the cumulative burden of chronic itch and skin lesions in PN.

Learn more about how chronic and systemic type 2 inflammation contributes to skin barrier dysfunction in atopic dermatitis
Prof. Vibeke Backer provides an insightful presentation on the association of type 2 inflammation and the pathogenesis and management of severe and uncontrolled CRSwNP.

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.

Unlock new perspectives on managing chronic airway diseases. Profs. Leonard Bacharier, Eugenio De Corso, Stella Lee, Marc Miravitlles, Celeste Porsbjerg, Klaus Rabe, and Martin Wagenmann – share their collective wisdom and experience on the evolving landscape of therapeutic strategies aimed at truly modifying disease progression, offering renewed hope for patients and practitioners alike.

Learn about the significant burden that patients with EoE experience, and the role of type 2 inflammation in this chronic, progressive disease.
Examine underlying type 2 inflammation as a driver of airway hyperresponsiveness in patients with asthma.