## Why IgG antibodies against Desmoglein 1 (Dsg1) is right Pemphigus foliaceus is characterized by autoimmune intraepidermal blistering caused by IgG autoantibodies against Desmoglein 1 (Dsg1), a desmosomal cadherin expressed predominantly in the superficial/granular layer of the epidermis. These antibodies disrupt desmosomal adhesion, leading to acantholysis (loss of cell-to-cell adhesion) in the superficial epidermis and creating the characteristic superficial subcorneal/granular layer split. The clinical presentation of superficial crusted erosions in seborrheic distribution without mucosal involvement, combined with the direct immunofluorescence pattern showing intercellular deposits in the superficial epidermis, is pathognomonic for PF with anti-Dsg1 serology (International Pemphigus Consensus 2019; Bolognia Dermatology 4th ed). ## Why each distractor is wrong - **IgG antibodies against Desmoglein 3 (Dsg3)**: This is the primary autoantigen in pemphigus vulgaris (PV), which causes suprabasal acantholysis and characteristically involves MUCOSAL lesions. The absence of mucosal involvement in this patient rules out PV and anti-Dsg3 antibodies. - **IgG antibodies against Desmoglein 1 and 3 (Dsg1 + Dsg3)**: This antibody profile is seen in pemphigus vulgaris with extensive skin involvement (mucocutaneous disease). This patient has no mucosal lesions, which is the defining clinical distinction of PF from PV. - **IgG antibodies against Desmoplakin II**: Desmoplakin is a plakin protein involved in desmosomal anchoring but is not the primary autoantigen in pemphigus foliaceus. Autoantibodies against desmoplakin are associated with paraneoplastic pemphigus, not PF. **High-Yield:** Anti-Dsg1 only = PF (superficial, no mucosa); Anti-Dsg3 ± Dsg1 = PV (suprabasal, mucosal involvement). [cite: International Pemphigus Consensus 2019; Bolognia Dermatology 4th ed]
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