Which mechanism best explains the abundant eosinophils seen within the blister cavity of bullous pemphigoid?

• A Direct cytotoxicity of anti-BP180 IgG on keratinocytes
• B IgE-mediated mast cell degranulation releasing eotaxin
• C Complement activation generating C5a, which is chemotactic for eosinophils ✓
• D Neutrophil elastase cleavage of hemidesmosomal proteins

Explanation

Binding of IgG to BP180 activates the classical complement pathway, generating B5a, an anaphylatoxin that attracts eosinophils into the blister. Eosinophil granule proteins such as major basic protein then degrade the dermoepidermal attachment complex, producing the subepidermal split. Neutrophil elastase is the dominant protease in linear IgA disease and mucous membrane pemphigoid, where neutrophils rather than eosinophils predominate.

Reference: Rook's Textbook of Dermatology, 9th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.