Autoimmune reactions are central to several skin disorders. In pemphigus vulgaris, autoantibodies target desmogleins in desmosomes, leading to acantholysis and blister formation. In bullous pemphigoid, autoantibodies attack hemidesmosomes, causing subepidermal blisters. Histologically, these conditions show intraepidermal and subepidermal clefting, respectively, along with inflammatory infiltrates.
