epidermolysis bullosa acquisita/edema

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Passive transfer of autoantibodies from a patient with mutilating epidermolysis bullosa acquisita induces specific alterations in the skin of neonatal mice.

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BACKGROUND Epidermolysis bullosa acquisita is a subepidermal bullous disease characterized by IgG autoantibodies directed against type VII collagen in anchoring fibrils. These autoantibodies are believed to play an important role in the pathogenesis of sub-lamina densa blister formation in this

Epidermolysis bullosa acquisita and inflammatory bowel disease.

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Immunologic studies on lesional and nonlesional "normal" -appearing skin of a 32-year-old man with epidermolysis bullosa acquisita (EBA) revealed the following: (1) Noninflammatory subepidermal bullae formation in the periodic acid-Schiff (PAS)-positive basement membrane; (2) linear deposits of

Conditional depletion of mast cells has no impact on the severity of experimental epidermolysis bullosa acquisita.

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The role of mast cells (MCs) in autoimmunity is the matter of an intensive scientific debate. Based on observations in different MC-deficient mouse strains, MCs are considered as fundamental players in autoimmune diseases. However, most recent data suggest that the outcome of such diseases is

Bullous systemic lupus erythematosus.

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Blistering eruptions are rare cutaneous manifestations of lupus erythematosus (LE) that may be caused by different mechanisms. Subepidermal clefting with frank vesiculation may occur in early lesions of chronic-, subacute-, and acute-cutaneous LE due to a severe vacuolar alteration of the

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