A 38-year-old African-American woman presents with chronic lesions on her cheeks, ears, and scalp. On examination, the structure marked **A** shows well-demarcated erythematous scaly plaques with central atrophic scarring and hypopigmented centers surrounded by hyperpigmented borders. Dermoscopy reveals follicular plugging, and histopathology shows hyperkeratosis with vacuolar interface change at the dermal-epidermal junction. Direct immunofluorescence demonstrates granular IgG and C3 deposition at the DEJ. Which of the following best describes the pathogenic mechanism underlying the erythematous scaly plaques marked **A** in this patient?

Explanation

## Why option 1 is correct The erythematous scaly plaques marked **A** in discoid lupus erythematosus (DLE) are the hallmark of T-cell mediated interface dermatitis. The pathogenesis involves UV-triggered, interferon-α-driven autoimmunity in genetically susceptible individuals (HLA-DR3/DR2), leading to apoptosis of basal keratinocytes and immune complex deposition at the dermal-epidermal junction. This mechanism is directly supported by the histopathologic findings (vacuolar interface change, perivascular lymphocytic infiltrate) and the positive lupus band test (granular IgG and C3 at the DEJ) seen in this patient. The EADV Guidelines CLE 2017 and Bolognia Dermatology 4th edition establish this as the core pathogenic mechanism of DLE. ## Why each distractor is wrong - **Option 2**: Neutrophil-mediated vasculitis is characteristic of leukocytoclastic vasculitis and other small-vessel vasculitides, not the interface dermatitis pattern of DLE. While immune complexes are deposited in DLE, the primary mechanism is T-cell mediated, not neutrophil-driven. - **Option 3**: Th2-driven eosinophilic infiltration with mast cell degranulation describes allergic contact dermatitis or atopic dermatitis, not the lymphocytic interface pattern of DLE. The infiltrate in DLE is predominantly T-lymphocytic and perivascular, not eosinophilic. - **Option 4**: While dyspigmentation (hypopigmentation and hyperpigmentation) is a cardinal feature of DLE lesions, the primary pathogenic mechanism is not selective melanocyte destruction. Dyspigmentation results from the interface dermatitis and subsequent epidermal atrophy, not from primary antibody-mediated melanocyte loss. **High-Yield:** DLE = T-cell mediated interface dermatitis (not vasculitis or type I hypersensitivity); UV + HLA susceptibility + IFN-α autoimmunity → basal keratinocyte apoptosis → scarring plaques on sun-exposed sites. [cite: EADV Guidelines CLE 2017; Bolognia Dermatology 4th ed]