In Toxic Epidermal Necrolysis (TEN), the key pathological event responsible for full-thickness epidermal detachment is:

• A Deposition of IgG antibodies against desmoglein-3
• B Keratinocyte apoptosis mediated by granulysin released by cytotoxic CD8+ T cells ✓
• C Complement-mediated lysis at the dermoepidermal junction
• D Neutrophil-mediated elastase activity dissolving keratinocyte attachments

Explanation

TEN is now understood to be primarily mediated by drug-specific CD8+ cytotoxic T lymphocytes that release granulysin, a cytotoxic protein that induces widespread keratinocyte apoptosis causing full-thickness epidermal necrosis and detachment. Granzyme B and perforin also contribute. This distinguishes TEN from pemphigus vulgaris (IgG against desmoglein-3 causing acantholysis) and bullous pemphigoid (complement-mediated at BMZ). Neutrophil elastase is not the primary mechanism.

Reference: Neena Khanna Illustrated Synopsis of Dermatology & STD, 6th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.