## Autoantigen Targets in Bullous Pemphigoid **Key Point:** Bullous pemphigoid is an autoimmune blistering disorder caused by IgG autoantibodies directed against hemidesmosomal antigens, specifically BP180 (collagen XVII) and BP230 (BPAG1). ### Mechanism of Autoantibody Action These autoantibodies target the hemidesmosomes, which are adhesion complexes at the dermal–epidermal junction (DEJ). The antibodies bind to the extracellular domains of these transmembrane and intracellular proteins, leading to: 1. Complement activation (C3 deposition) 2. Recruitment of inflammatory cells 3. Release of proteolytic enzymes 4. Disruption of the hemidesmosomal attachment 5. Subepidermal blister formation ### Distinction from Pemphigus Vulgaris | Feature | Bullous Pemphigoid | Pemphigus Vulgaris | |---------|-------------------|-------------------| | **Autoantigen** | BP180, BP230 (hemidesmosomal) | Desmoglein 1, 3 (desmosomal) | | **Blister level** | Subepidermal | Intraepidermal (acantholysis) | | **Antibody type** | IgG, IgE | IgG | | **Immunofluorescence** | Linear IgG/C3 at DEJ | Intercellular IgG ("tombstone") | **High-Yield:** BP180 is the most common target antigen; anti-BP180 seropositivity correlates with disease activity and is present in ~80% of BP patients. **Clinical Pearl:** The presence of circulating IgE antibodies against BP180 in some BP patients may contribute to mast cell activation and eosinophilic infiltration in the blister cavity. 
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