A 28-year-old woman presents with a 10-day history of painful oral erosions, conjunctivitis, and symmetric target lesions on her dorsal hands and extensor forearms. She reports a history of recurrent herpes labialis 7–10 days prior to each flare. Examination reveals three-zone target lesions (<3 cm), involvement of two mucosae (oral and ocular), and negative Nikolsky sign. The condition marked **B** in the diagram is suspected. Which of the following best describes the pathophysiologic mechanism underlying this condition?
A. Immediate-type hypersensitivity with mast cell degranulation and IgE-mediated immune response
B. T-cell mediated delayed-type hypersensitivity against viral antigens with CD8+ T cell-driven keratinocyte apoptosis
C. Direct viral invasion of keratinocytes with subsequent epidermal necrosis
D. Neutrophilic infiltration with formation of immune complexes in dermal vessels
Explanation
Why "T-cell mediated delayed-type hypersensitivity against viral antigens with CD8+ T cell-driven keratinocyte apoptosis" is right
The condition marked B (Erythema Multiforme Major) is fundamentally an immune-mediated mucocutaneous reaction driven by T-cell delayed-type hypersensitivity. The pathophysiology involves CD8+ T cells recognizing viral antigens (particularly HSV DNA fragments) deposited in the skin, leading to production of interferon-gamma (IFN-γ) and subsequent keratinocyte apoptosis. This mechanism explains the distinctive target lesions with central necrosis and the clinical presentation of EM major with severe mucosal involvement and systemic symptoms, as described in Bolognia and Fitzpatrick's dermatology texts.
Why each distractor is wrong
Immediate-type hypersensitivity with mast cell degranulation and IgE-mediated immune response: This describes acute urticaria or anaphylaxis, not EM. While urticaria multiforme may present with urticarial lesions, EM major is characterized by true target lesions and is T-cell mediated, not IgE-mediated.
Neutrophilic infiltration with formation of immune complexes in dermal vessels: This mechanism is more consistent with vasculitis or immune complex-mediated reactions (e.g., serum sickness-like reactions). EM major is characterized by lymphocytic infiltrate and interface dermatitis on histology, not prominent neutrophilic vasculitis.
Direct viral invasion of keratinocytes with subsequent epidermal necrosis: While HSV is the most common trigger, EM is not caused by direct viral cytopathic effect. Rather, it is the immune response to viral antigens that drives the condition. This distinction is critical: EM is immune-mediated, not infectious in the direct sense.
High-YieldNEET PG
EM major is a T-cell mediated delayed-type hypersensitivity reaction (most commonly HSV-triggered), characterized by target lesions, severe mucosal involvement (≥2 mucosae), and negative Nikolsky sign—distinguishing it from SJS/TEN which are drug-induced and have positive Nikolsky sign.
Bolognia Dermatology 5e; Fitzpatrick's 9e Chapter 43
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