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Previous Volume 355:1800-1810 October 26, 2006 Number 17 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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Pemphigus, which is caused by autoantibodies, and bullous impetigo (including its generalized form, the staphylococcal scalded-skin syndrome), which is caused by Staphylococcus aureus, are seemingly unrelated diseases. However, 200 years ago, astute clinicians realized that these diseases had enough clinical similarities to call bullous impetigo and the scalded-skin syndrome in infants "pemphigus neonatorum."^1,2 In this review we explain how a common mechanism accounts for the clinical overlap of these blistering diseases of the skin, and how the unraveling of the molecular pathophysiology of pemphigus provided the clues that were necessary to determine the mechanism of the formation of blisters in . . . [Full Text of this Article]

Pemphigus

Desmogleins

Pathogenicity of Antidesmoglein Antibodies

Desmoglein Compensation

Pemphigus Autoantibodies and Loss of Adhesion of Keratinocytes

Inactivation of Desmoglein

Direct and Indirect Effects of Pemphigus Antibodies

Bullous Impetigo and the Staphylococcal Scalded-Skin Syndrome

Pemphigus Neonatorum

Production of Exfoliative Toxin by Staphylococcus

Diagnosis and Therapy

Bullous Impetigo and the Staphylococcal Scalded-Skin Syndrome

Pemphigus

Conclusions

Source Information

From the Departments of Dermatology, University of Pennsylvania School of Medicine, Philadelphia (J.R.S.); and Keio University School of Medicine, Tokyo (M.A.).

Address reprint requests to Dr. Stanley at the University of Pennsylvania, 211 CRB, 415 Curie Blvd., Philadelphia, PA 19104.

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• Spindler, V., Drenckhahn, D., Zillikens, D., Waschke, J. (2007). Pemphigus IgG Causes Skin Splitting in the Presence of Both Desmoglein 1 and Desmoglein 3. Am. J. Pathol. 171: 906-916 [Abstract] [Full Text]  
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