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Published on: May 18, 2010
An attempt to develop mouse model for anti-laminin γ1 pemphigoid
Hiroshi Koga1, Norito Ishii, Teruki Dainichi
1Department of Dermatology, Kurume University School of Medicine, and Kurume University Institute of Cutaneous Cell Biology, Kurume, Japan.
Journal of Dermatological Science
|February 16, 2013
Summary
Researchers developed mouse models for anti-laminin γ1 pemphigoid. While antibodies bound the skin basement membrane, neither model produced blisters, indicating further refinement is needed to replicate skin lesions.
Area of Science:
- Dermatology
- Immunology
- Autoimmune Blistering Diseases
Background:
- Autoantibodies in anti-p200 pemphigoid target laminin γ1, defining anti-laminin γ1 pemphigoid.
- The role of anti-laminin γ1 autoantibodies, especially to the C-terminal integrin binding site, in causing subepidermal blisters remains unclear.
Purpose of the Study:
- To develop and evaluate animal models for anti-laminin γ1 pemphigoid.
Main Methods:
- Two mouse models were created: a passive transfer model using rabbit IgG against murine laminin γ1 C-terminus and an active disease model involving direct immunization with the recombinant protein.
- Immunoblotting confirmed patient sera reactivity with human laminin γ1 C-terminus.
Main Results:
- Rabbit IgG deposited at the epidermal basement membrane zone in the passive transfer model, without C3 deposition.
- No IgG or C3 deposition was observed in the active disease model.
- Neither model exhibited phenotypic or histopathological signs of blister formation.
Conclusions:
- Developed mouse models for anti-laminin γ1 pemphigoid, with antibody binding observed in the passive transfer model.
- The models failed to reproduce skin lesions, highlighting the need for further improvements to accurately mimic the disease.