Professor Mona Bafadhel presents a comprehensive overview of type 2 inflammation in COPD, exploring its underlying mechanisms, clinical manifestations, and implications for patient outcomes.

Learn about key drivers of type 2 inflammation in EoE and how they mediate progressive esophageal remodeling and impact patient burden

Join Drs. Nicola Hanania, Surya Bhatt, and Celeste Porsbjerg for a session exploring the burden of COPD in patients with type 2 inflammation and review key cytokine pathways and Phase 3 data on emerging biologic therapies.

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.

Join Profs. Dave Singh and Klaus Rabe as they examine the clinical relevance of exacerbations, lung function, symptoms, quality of life, and comorbidities in COPD, as well as the evolving concept of disease stability and what that could mean for treatment planning and the future of COPD care.

Join Dr. Kwatra outlining the micro itch cycle involving type 2 cell polarization and cytokines that directly affect fibroblasts to cause more immune dysregulation in PN.

Join Dr Kwatra as he dives deeper into the mechanism of lesion formation in Prurigo Nodularis and the impact the development of these skin lesions have on patient life.

Dr. Sonja Ständer and Dr. Shawn Kwatra discuss the unique features of prurigo nodularis (PN) as well as the characteristics that are shared with atopic dermatitis, and aim to raise awareness of PN among both physicians and patients.

Dr. Ramien explores the concept of disease modification in AD focusing on disease control, and the prevention or slowing of development of atopic comorbidities.

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.