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Session Information

DSG D006 - Advances in Pemphigus & Pemphigoid

Open admission to eligible categories, no tuition or ticket


Date: Saturday, March 02

CME Credits: 2.00

Location: Room C219

Time: 3:30 PM - 5:30 PM

Director: Luis A. Diaz, MD, FAAD - Handout

Learning Objectives:
Following this course, the attendee should be able to:

  • Discuss the pathogenesis of pemphigus and pemphigoid
  • Formulate the best treatment for these patients

Structural skin molecules are targeted by “pathogenic” autoantibodies which are known to induce intra-epidermal and subepidermal blisters in experimental animals. In pemphigus vulgaris and pemphigus foliaceus, desmosomal antigens, i.e., Dsg3 and Dsg1 respectively, are the targets. In bullous pemphigoid hemidesmosomal antigens, i.e., BP230 and BP180, are bound by these autoantibodies. These pathogenic autoantibodies may trigger blister formation by different mechanisms, e.g., signal transduction, apoptosis or inflammation. Therapies aimed at eliminating pathogenic autoantibodies from these patients will be discussed.