Mechanism of lesion production in pemphigus and pemphigoid.
Current evidence strongly supports the theory that the lesions of pemphigus are due to binding of pemphigus antibody to an antigen in or near the epidermal cell membrane, which causes a release of at least one enzyme which results in dissolution of the intercellular attachments and acantholysis. Similarly, strong evidence supports the hypothesis that pemphigoid blisters are due to binding of antibody at the basement membrane, followed by activation of complement and release of anaphylatoxins which activate tissue mast cells to release eosinophil chemotactic factor. These eosinophils then release tissue-destructive enzymes and reactive oxygen intermediates directly onto the basement membrane zone, with loss of dermoepidermal adherence and formation of blisters.
D000906:Antibodies; D000941:Antigens; D001485:Basement Membrane / Q000276:immunology; D003165:Complement System Proteins; D004789:Enzyme Activation; D006801:Humans; D007962:Leukocytes / Q000276:immunology; D008407:Mast Cells / Q000276:immunology; D010391:Pemphigoid, Bullous / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D010392:Pemphigus / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D012867:Skin / Q000276:immunology / Q000473:pathology; D012872:Skin Diseases, Vesiculobullous / Q000209:etiology*
D000906:Antibodies; D000941:Antigens; D003165:Complement System Proteins