In bullous pemphigoid, which cell-adhesion structure is targeted by autoantibodies?

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Multiple Choice

In bullous pemphigoid, which cell-adhesion structure is targeted by autoantibodies?

Explanation:
Autoantibodies in bullous pemphigoid target the adhesion structures that attach basal keratinocytes to the basement membrane: hemidesmosomes. These complexes link the epidermis to the underlying dermis, and their disruption leads to a split at the dermal-epidermal junction with subepidermal blister formation. Hemidesmosomes involve components such as BP180 (type XVII collagen) and BP230, which are the common autoantibody targets in this disease. In contrast, desmosomes mediate cell-to-cell adhesion within the epidermis; antibodies against desmogleins cause intraepidermal blisters (as seen in other blistering disorders). Gap junctions and tight junctions are not the primary adhesion systems involved in this pattern of blistering, so targeting them wouldn’t explain the typical subepidermal blisters of bullous pemphigoid.

Autoantibodies in bullous pemphigoid target the adhesion structures that attach basal keratinocytes to the basement membrane: hemidesmosomes. These complexes link the epidermis to the underlying dermis, and their disruption leads to a split at the dermal-epidermal junction with subepidermal blister formation. Hemidesmosomes involve components such as BP180 (type XVII collagen) and BP230, which are the common autoantibody targets in this disease.

In contrast, desmosomes mediate cell-to-cell adhesion within the epidermis; antibodies against desmogleins cause intraepidermal blisters (as seen in other blistering disorders). Gap junctions and tight junctions are not the primary adhesion systems involved in this pattern of blistering, so targeting them wouldn’t explain the typical subepidermal blisters of bullous pemphigoid.

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