: Often the first sign in infancy, caused by skin barrier defects (e.g., filaggrin mutations) that allow for epicutaneous allergen sensitization.
: These cells produce cytokines (IL-4, IL-13) that trigger B cells to differentiate into plasma cells producing allergen-specific IgE. : Often the first sign in infancy, caused
: Upon re-exposure, allergens cross-link IgE on the surface of mast cells, causing degranulation and the release of inflammatory mediators like histamine and leukotrienes. 2. The Atopic March The core of atopy is a Type I
While there is currently no cure, management focuses on controlling inflammation and restoring barrier function. Atopy - StatPearls - NCBI Bookshelf - NIH activating TH2 or ILC2 cells.
: Antigen-presenting cells perceive allergens (like pollen or dust mites) as danger signals, activating TH2 or ILC2 cells.
The core of atopy is a Type I hypersensitivity reaction driven by a Type 2 immune response.
: Sensitization through inflamed skin can lead to early-onset food allergies.