## Autoantigen in Pemphigus Vulgaris **Key Point:** Pemphigus vulgaris is characterized by IgG autoantibodies directed against desmogleins, which are transmembrane glycoproteins that mediate cell-to-cell adhesion in the epidermis. ### Desmoglein Specificity | Feature | Desmoglein 3 | Desmoglein 1 | |---------|--------------|---------------| | **Location** | Lower epidermis (basal & suprabasal layers) | Upper epidermis (superficial layers) | | **Antibody Presence** | Present in all PV cases | Present in ~50% of PV cases | | **Clinical Correlation** | Mucosal involvement; oral erosions | Cutaneous involvement; facial/trunk lesions | **High-Yield:** Anti-Desmoglein 3 (Dsg3) antibodies are **pathognomonic** for pemphigus vulgaris and are found in 100% of cases. Anti-Desmoglein 1 (Dsg1) antibodies correlate with extent of cutaneous disease. ### Mechanism of Acantholysis IgG autoantibodies bind to desmogleins → disruption of desmosomal adhesion → loss of cell-to-cell contact (acantholysis) → intraepidermal blister formation. **Clinical Pearl:** The presence of **anti-Dsg3 alone** predicts mucosal-dominant disease, while **anti-Dsg3 + anti-Dsg1** predicts mucocutaneous disease. **Mnemonic:** **DES**moglein = **DES**mosomal adhesion molecule. Pemphigus = **intra**-epidermal blistering due to loss of desmoglein-mediated cell adhesion. 
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