A 32-year-old Indian woman presents with a 6-month history of progressive scarring alopecia of the scalp and well-demarcated erythematous plaques on the face and ears. On examination, the plaques show central atrophy with adherent scale that, when lifted, reveals keratotic spikes from follicular ostia. The structure marked **A** in the diagram represents these characteristic scarring photodistributed plaques with follicular plugging. Which of the following statements about the pathogenesis of this lesion is most accurate?
A. Type IV cytotoxic T-cell mediated autoimmune attack on basal keratinocytes triggered by UV light and other factors in genetically susceptible individuals
B. Direct antibody-mediated destruction of melanocytes resulting in dyspigmentation and scarring
C. Type I hypersensitivity reaction to antimalarial drugs causing follicular occlusion
D. Type II immune complex deposition at the dermoepidermal junction leading to complement-mediated tissue destruction
Explanation
Why Type IV cytotoxic T-cell mediated autoimmune attack is right
Discoid lupus erythematosus (DLE) is characterized by a Type IV cytotoxic T-cell mediated pathogenesis with an interferon-α/type I interferon signature. The autoimmune attack targets basal keratinocytes and is triggered by UV light, smoking, drugs, and hormonal factors in genetically susceptible individuals. This mechanism explains the photodistributed nature of the lesions and the characteristic follicular plugging seen in the structure marked A. The histology shows interface dermatitis with basal vacuolar degeneration and periadnexal lymphocytic infiltrate, consistent with T-cell mediated injury (Harrison's 21e Ch 358; Bolognia 5e Ch 41).
Why each distractor is wrong
Type II immune complex deposition: While lupus band (granular IgG/IgM/C3 at the dermoepidermal junction) is seen on direct immunofluorescence in 90% of lesional DLE skin, the PRIMARY pathogenic mechanism is T-cell mediated, not immune complex-driven. Immune complexes are a secondary finding.
Type I hypersensitivity to antimalarials: Antimalarials (hydroxychloroquine) are the FIRST-LINE TREATMENT for DLE, not a cause. Patients do not develop hypersensitivity to the therapeutic agent; rather, antimalarials suppress the disease by reducing interferon-α production.
Direct antibody-mediated destruction of melanocytes: While dyspigmentation (central hypopigmentation with peripheral hyperpigmentation) is a characteristic feature of DLE, it results from the interface dermatitis and basal cell damage, not from direct anti-melanocyte antibodies. The dyspigmentation is secondary to the T-cell mediated basal keratinocyte injury.
High-YieldNEET PG
DLE is Type IV T-cell mediated (not immune complex), ANA may be low-titer or negative, and only 5-10% progress to systemic SLE—making it the mildest form of cutaneous lupus.
Harrison's 21e Ch 358; Bolognia 5e Ch 41
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