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Related Concept Videos

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Membrane lipids such as phosphatidylinositol (PI) are precursors for several membrane-bound and soluble second messengers. Specific kinases phosphorylate PI and produce phosphorylated inositol phospholipids. One such inositol phospholipids are the  phosphatidylinositol-4,5 bisphosphate [PI(4,5)P2], present in the inner half of the lipid bilayer. Upon ligand binding, GPCR stimulates Gq proteins to turn on phospholipase Cꞵ. Activated phospholipase Cꞵ cleaves PI(4,5)P2 and...
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A Dsg3-specific pemphigus autoantibody induces formation of immature desmosomes associated with impaired adhesion.

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Related Experiment Video

Updated: Jul 31, 2025

Granulocyte-dependent Autoantibody-induced Skin Blistering
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Dsg3 epitope-specific signalling in pemphigus.

Thomas Schmitt1, Christoph Hudemann2, Sina Moztarzadeh1

  • 1Instiute of Anatomy, Faculty of Medicine, Chair of Vegetative Anatomy, Ludwig-Maximilian -Universität (LMU) Munich, München, Germany.

Frontiers in Immunology
|May 5, 2023
PubMed
Summary
This summary is machine-generated.

Pemphigus autoantibodies targeting different desmoglein 3 (Dsg3) epitopes trigger distinct signaling pathways. AK23, targeting the EC1 domain, caused Dsg3 depletion and activated Src, unlike 2G4 which targeted the EC5 domain.

Keywords:
adhesionautoimmune diseasedesmoglein (dsg)desmosomesepidermiskeratinpemphigusskin

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Area of Science:

  • Immunodermatology
  • Cellular Biology
  • Molecular Signaling

Background:

  • Pemphigus is an autoimmune blistering disease affecting skin and mucous membranes.
  • Disease phenotype correlates with autoantibody targets, primarily desmogleins (Dsgs).
  • Pathogenicity of autoantibodies can depend on the specific epitope targeted on Dsgs.

Purpose of the Study:

  • To investigate epitope-specific signaling induced by anti-Dsg3 autoantibodies in pemphigus.
  • To compare the effects of two pathogenic murine IgGs, 2G4 (anti-EC5 Dsg3) and AK23 (anti-EC1 Dsg3).

Main Methods:

  • Dispase-based dissociation assay
  • Western Blot analysis
  • Stimulated emission depletion (STED) microscopy
  • Ca2+ flux measurements
  • G-Protein-linked immunosorbent assay (ELISA)

Main Results:

  • AK23 induced greater loss of cell adhesion than 2G4.
  • Both antibodies caused keratin retraction and reduced desmosome numbers.
  • Only AK23 induced Dsg3 depletion, p38MAPK and Akt phosphorylation, and Src phosphorylation.
  • Src and Akt activation were dependent on p38MAPK; inhibition rescued pathogenic effects.

Conclusions:

  • Pemphigus autoantibodies against Dsg3 induce epitope-specific signaling pathways.
  • Dsg3 depletion is linked to specific signaling events, potentially mediated by p38MAPK and Src.
  • Understanding these pathways offers insights into pemphigus pathogenesis.