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[Cell adhesion molecules and extracellular matrix components as target structures of autoimmunity]
1Institut für Pathologie, Martin-Luther-Universität Halle-Wittenberg, Saale.
Verhandlungen Der Deutschen Gesellschaft Fur Pathologie
|January 1, 1996
Summary
Autoimmune blistering diseases stem from autoantibodies targeting cell adhesion molecules. Understanding these molecular targets, like desmogleins and collagen VII, is key to developing new therapies for skin blistering conditions.
Area of Science:
- Immunodermatology
- Molecular Biology
- Autoimmunity
Context:
- Cell-cell and cell-matrix adhesion molecules are targets of antibody-mediated autoimmunity.
- Autoantibodies against these molecules cause disturbances in cell and tissue adhesion, leading to blistering diseases.
- Recent molecular characterization has elucidated key autoantigens involved.
Purpose:
- To review molecular targets of autoantibodies in blistering diseases.
- To link specific autoantigens to distinct clinical manifestations.
- To highlight the pathogenic relevance of autoantibodies in various (muco-)cutaneous blistering conditions.
Summary:
- Desmosomal cadherins (desmogleins, desmocollins) mediate epidermal adhesion; autoantibodies against desmoglein 1 and 3 cause pemphigus foliaceus and vulgaris, respectively.
- Hemidesmosome components BPAG1 and BPAG2 are autoantigens in bullous pemphigoid and pemphigoid gestations.
- Autoantibodies against laminin 5, collagen type VII, and collagen type IV are implicated in cicatricial pemphigoid, epidermolysis bullosa acquisita, and Goodpasture's syndrome.
Impact:
- Provides a molecular basis for understanding blistering diseases.
- Identifies specific autoantigens for diagnostic and therapeutic advancements.
- Suggests potential for developing novel therapeutic strategies targeting these autoimmune mechanisms.