In cicatricial pemphigoid with ocular involvement, the primary immune mechanism differs from pemphigus vulgaris in that it involves:

• A IgG and IgA antibodies against BP180 (BPAG2) at the dermoepidermal junction causing subepithelial blistering ✓
• B IgG antibodies against desmoglein-3 causing intraepithelial acantholysis
• C T-cell-mediated cytotoxicity against conjunctival basal cells
• D Complement-mediated lysis of goblet cells

Explanation

Ocular cicatricial pemphigoid (mucous membrane pemphigoid) involves autoantibodies — primarily IgG and IgA — targeting the hemidesmosomal components of the basement membrane zone, most importantly BP180 (BPAG2/type XVII collagen) and beta-4 integrin. This produces subepithelial blistering and subsequent fibrosis and cicatrisation. In contrast, pemphigus vulgaris involves IgG antibodies against desmoglein-3 (and -1), causing suprabasal intraepithelial acantholysis. Ocular cicatricial pemphigoid progresses through stages (Foster classification) leading to symblepharon, entropion, trichiasis, ankyloblepharon, and limbal stem cell deficiency. Dapsone and systemic immunosuppression (cyclophosphamide, mycophenolate) are mainstays.

Reference: Khurana Comprehensive Ophthalmology, 7th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.