A 32-year-old woman presents with acute onset urticaria and angioedema 15 minutes after consuming peanuts at a restaurant. She has a history of similar reactions to tree nuts and shellfish. Which of the following is the most common immunological mechanism underlying her food allergy?

Explanation

## Immunological Mechanism of IgE-Mediated Food Allergy **Key Point:** IgE-mediated hypersensitivity (Type I) is the most common mechanism underlying acute food allergies, accounting for approximately 90% of food-induced anaphylaxis cases. ### Pathophysiology The reaction occurs in two phases: 1. **Sensitization Phase** - Allergen (peanut protein) is processed by antigen-presenting cells - Th2 cells are activated, promoting IL-4 and IL-5 production - B cells differentiate into plasma cells secreting allergen-specific IgE - IgE binds to high-affinity receptors (FcεRI) on mast cells and basophils 2. **Reaction Phase (upon re-exposure)** - Cross-linking of IgE on mast cell surface by allergen - Rapid degranulation releasing preformed mediators (histamine, tryptase, heparin) - Release of newly synthesized mediators (leukotrienes, prostaglandins, PAF) - Clinical manifestations within minutes: urticaria, angioedema, bronchospasm, anaphylaxis **High-Yield:** The **speed of onset** (15 minutes in this case) is pathognomonic for IgE-mediated hypersensitivity. Delayed hypersensitivity reactions typically manifest 24–72 hours after exposure. ### Clinical Features Supporting Type I Hypersensitivity | Feature | Type I (IgE) | Type III (IgG) | Type IV (T-cell) | |---------|-------------|----------------|------------------| | **Onset** | Minutes to 2 hours | 3–10 hours | 24–72 hours | | **Mediators** | Histamine, leukotrienes, PAF | Immune complexes, complement | Cytokines, cell-mediated | | **Skin findings** | Urticaria, angioedema | Vasculitis, purpura | Eczema, lichenification | | **Anaphylaxis** | Yes, common | Rare | No | **Clinical Pearl:** The patient's history of multiple food allergies (peanuts, tree nuts, shellfish) with acute urticaria and angioedema is classic for atopic syndrome — a genetic predisposition to mount exaggerated Th2 responses and produce elevated IgE. **Mnemonic:** **FAST** = Food Allergy Systemic Type I - **F**ast onset (minutes) - **A**cute urticaria/angioedema - **S**ensitization phase precedes reaction - **T**ype I hypersensitivity (IgE-mediated) ### Why Other Mechanisms Are Less Common in Acute Food Allergy - **IgG immune complexes (Type III):** Cause serum sickness-like reactions (3–10 hours post-exposure), vasculitis, and arthralgia — not the immediate urticaria seen here. - **T-cell mediated (Type IV):** Delayed onset (24–72 hours), associated with contact dermatitis and food-protein-induced enterocolitis syndrome (FPIES) in infants, not acute anaphylaxis. - **IgA-mediated:** Primarily involved in IgA nephropathy and celiac disease; not a primary mechanism in acute food allergy. [cite:Robbins 10e Ch 6]