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Type 2 Inflammation
Understanding the Pathophysiology of Pediatric Type 2 Inflammatory Diseases
Prof. Oscar Palomares discusses the underlying pathophysiology of type 2 inflammation in pediatric patients with AD, asthma, or EoE.
PhD
Oscar Palomares
Learning objectives
Evaluate the key and central role of IL-4 and IL-13 in local and systemic effects of disease pathology, and the role of IL-4 in driving type 2 amplification and chronicity of disease progression
Understand the importance of understanding potential disease trajectories in pediatric patients, and the onset and persistence of type 2 inflammation
Description
Join global expert Oscar Palomares, PhD, as he discusses the shared and distinct elements of underlying type 2 pathophysiology in atopic dermatitis (AD), asthma, and eosinophilic esophagitis (EoE).
ADVENT is a global medical education non-promotional program by Sanofi and Regeneron. This website is intended only for duly authenticated healthcare professionals in Algeria, Argentina, Australia, Austria, Bahrain, Belgium, Brazil, Bulgaria, Canada, Chile, China, Colombia, Costa Rica, Croatia, Czech Republic, Denmark, Dominican Republic, Ecuador, Egypt, Estonia, Finland, France, Germany, Greece, Guatemala, Hong Kong, Hungary, Iceland, India, Israel, Italy, Japan, Kuwait, Latvia, Lebanon, Lithuania, Macau, Malaysia, Norway, Oman, Panama, Peru, Poland, Portugal, Qatar, Romania, Saudi Arabia, Singapore, Slovenia, South Africa, South Korea, Spain, Sudan, Sweden, Switzerland, Taiwan, Thailand, The Netherlands, Turkey, United Arab Emirates, or the United States of America.
For healthcare professionals in Algeria: Please read the additional Terms of Use.
Sanofi and Regeneron are global leaders in pharmaceutical development, each with a long history of supporting frontline physicians to improve human health and reduce the burden of disease. Driven by the same commitment to patients and their families, Sanofi and Regeneron have partnered to take on type 2 inflammation and the range of chronic conditions in which excessive inflammation plays a role.