Pemphigus vulgaris involves autoantibodies against desmoglein in the skin. Which Type II mechanism does this illustrate?

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Multiple Choice

Pemphigus vulgaris involves autoantibodies against desmoglein in the skin. Which Type II mechanism does this illustrate?

Explanation:
Type II hypersensitivity is antibody-mediated effects on cell surfaces or extracellular structures. In pemphigus vulgaris, IgG autoantibodies bind to desmoglein in desmosomes between skin cells, directly disrupting cell–cell adhesion and causing loss of cohesion (acantholysis) with resulting flaccid bullae. This direct interference with a cell-surface adhesion molecule exemplifies antibody-mediated disruption of cell adhesion. Immune complex deposition in vessels is type III, T cell–mediated cytotoxicity is type IV, and IgE-mediated mast cell degranulation is type I, which explains why those options don’t fit this mechanism.

Type II hypersensitivity is antibody-mediated effects on cell surfaces or extracellular structures. In pemphigus vulgaris, IgG autoantibodies bind to desmoglein in desmosomes between skin cells, directly disrupting cell–cell adhesion and causing loss of cohesion (acantholysis) with resulting flaccid bullae. This direct interference with a cell-surface adhesion molecule exemplifies antibody-mediated disruption of cell adhesion.

Immune complex deposition in vessels is type III, T cell–mediated cytotoxicity is type IV, and IgE-mediated mast cell degranulation is type I, which explains why those options don’t fit this mechanism.

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