Type I Hypersensitivity (IgE-Mediated)

Type I hypersensitivity is an immediate, IgE-mediated immune reaction that occurs upon re-exposure to a sensitizing allergen.

Examples:

Phase 1 – Sensitization (First Exposure)

Initial exposure does NOT usually produce symptoms.

Step-by-step: 

1) Allergen enters tissue (pollen, food protein, etc.)
2) Dendritic cells process and present antigen via MHC II
3) Naïve CD4+ T cells differentiate into Th2 cells
4) Th2 cells release:
     * IL-4 → Class switching to IgE
     * IL-13 → IgE production and mucus production
     * IL-5 → Eosinophil activation
5) B cells produce allergen-specific IgE
6) IgE binds FcεRI receptors on mast cells and basophils

Result: 

Mast cells are now "armed" with allergen-specific IgE.

No symptoms yet.

Phase 2 – Re-Exposure (Effector Phase)

Upon re-exposure: 

1) Allergen cross-links IgE molecules on mast cell surface
2) Calcium influx occurs
3) Rapid degranulation

This produces the immediate allergic reaction.

Early Phase Reaction (Minutes)

Mediators released:

Physiologic effects:

Clinical examples:

Primary drug target:

Late Phase Reaction (Hours)

Occurs 4–8 hours after initial reaction.

Mediated by:

Effects:

Primary drug target:

Systemic Type I Reaction – Anaphylaxis

When mediator release becomes systemic:

First-line treatment:

See:

Key Immunologic Components

Component Role
IgE Binds mast cells and basophils
FcεRI receptor High-affinity IgE receptor
Th2 cells Drive IgE production
IL-4 / IL-13 Promote class switching to IgE
IL-5 Eosinophil recruitment
Mast cells Immediate mediator release
Eosinophils Late-phase inflammation

Contrast With Other Hypersensitivity Types

Type Mechanism Example
I IgE-mediated Anaphylaxis
II IgG/IgM against cell surface Hemolytic anemia
III Immune complex deposition Serum sickness
IV T-cell mediated (delayed) Contact dermatitis

See:

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