Pemphigus. Verlust des desmosomalen zell-zell-kontaktes

Translated title of the contribution: Pemphigus: Loss of desmosomal cell-cell adhesion

Enno Schmidt, Eva Bettina Bröcker, Detlef Zillikens*

*Corresponding author for this work
25 Citations (Scopus)


Pemphigus diseases comprise a group of autoimmune disorders which are characterized by intraepidermal blisters and autoantibodies to components of desmosomes. Desmosomes mediate adhesion between neighbouring keratinocytes. A common feature of pemphigus diseases are intercellular deposits of IgG or, less frequently, of IgA within the epidermis. The group of pemphigus diseases includes pemphigus vulgaris, pemphigus foliaceus, pemphigus vegetans, pemphigus herpetiformis, pemphigus erythematosus, paraneoplastic pemphigus, drug-induced pemphigus, and IgA pemphigus. Using molecular tools, some of the autoantigens in these diseases have been characterized. In pemphigus vulgaris, autoantibodies are directed to desmoglein 3 and in pemphigus foliaceus to desmoglein 1. Target antigens in IgA pemphigus are desmocollin 1 and desmoglein 3. In paraneoplastic pemphigus, autoantibodies react with a complex of various proteins, including desmoplakin 1 and 2, BP230, envoplakin, periplakin, plectin, desmoglein 3, and a yet uncharacterized 170 kD protein. This review summarizes new insights into the immunopathogenesis and diagnosis of pemphigus diseases.

Translated title of the contributionPemphigus: Loss of desmosomal cell-cell adhesion
Original languageGerman
Issue number5
Pages (from-to)309-318
Number of pages10
Publication statusPublished - 05.2000

Research Areas and Centers

  • Academic Focus: Center for Infection and Inflammation Research (ZIEL)


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