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Published in: Archives of Dermatological Research 1/2007

Open Access 01-04-2007 | Review Article

The relevance of the IgG subclass of autoantibodies for blister induction in autoimmune bullous skin diseases

Authors: Cassian Sitaru, Sidonia Mihai, Detlef Zillikens

Published in: Archives of Dermatological Research | Issue 1/2007

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Abstract

Autoimmune bullous skin diseases are characterized by autoantibodies and T cells specific to structural proteins maintaining cell–cell and cell–matrix adhesion in the skin. Existing clinical and experimental evidence generally supports a pathogenic role of autoantibodies for blister formation. These autoantibodies belong to several IgG subclasses, which associate with different functional properties and may thus determine the pathogenic potential of IgG antibodies. In pemphigus diseases, binding of IgG to keratinocytes is sufficient to cause intraepidermal blisters without engaging innate immune effectors and IgG4 autoantibodies seem to mainly mediate acantholysis. In contrast, in most subepidermal autoimmune blistering diseases, complement activation and recruitment and activation of leukocytes by autoantibodies are required for blister induction. In these conditions, tissue damage is thought to be mainly mediated by IgG1, but not IgG4 autoantibodies. This review summarizes the current knowledge on the pathogenic relevance of the IgG subclass of autoantibodies for blister formation. Characterization of the pathogenically relevant subclass(es) of autoantibodies not only provides mechanistic insights, but should greatly facilitate the development of improved therapeutic modalities of autoimmune blistering diseases.
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Metadata
Title
The relevance of the IgG subclass of autoantibodies for blister induction in autoimmune bullous skin diseases
Authors
Cassian Sitaru
Sidonia Mihai
Detlef Zillikens
Publication date
01-04-2007
Publisher
Springer-Verlag
Published in
Archives of Dermatological Research / Issue 1/2007
Print ISSN: 0340-3696
Electronic ISSN: 1432-069X
DOI
https://doi.org/10.1007/s00403-007-0734-0

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