An attempt to develop mouse model for anti-laminin γ1 pemphigoid
| Autor: | Tadashi Karashima, Hiroshi Koga, Takashi Hashimoto, Takahiro Hamada, Chika Ohata, Teruki Dainichi, Norito Ishii, Minao Furumura, Daisuke Tsuruta |
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| Rok vydání: | 2013 |
| Předmět: |
Pemphigoid
Dermatology Immunofluorescence Biochemistry Immunoglobulin G Mice Laminin Pemphigoid Bullous medicine Animals Humans Amino Acids Molecular Biology Autoantibodies Integrin binding Dermoepidermal junction Mice Knockout Mice Inbred BALB C integumentary system biology medicine.diagnostic_test Chemistry Pemphigus vulgaris Immunization Passive medicine.disease Molecular biology Recombinant Proteins Mice Inbred C57BL Disease Models Animal Immunity Active Immunology biology.protein Rabbits Bullous pemphigoid |
| Zdroj: | Journal of Dermatological Science. 70:108-115 |
| ISSN: | 0923-1811 |
| DOI: | 10.1016/j.jdermsci.2013.01.001 |
| Popis: | Background We recently reported that the autoantibodies of anti-p200 pemphigoid sera react with laminin γ1 and renamed this entity as anti-laminin γ1 pemphigoid. However, it has not been clarified whether the anti-laminin γ1 autoantibodies, particularly those to the C-terminal integrin binding site, affect the dermoepidermal junction and cause subepidermal blisters. Objective The aim of this study was to develop animal models for anti-laminin γ1 pemphigoid. Methods We attempted to produce two mouse models for anti-laminin γ1 pemphigoid; (1) a passive transfer model: injection of rabbit IgG to shorter bacterial recombinant protein of the murine laminin γ1 C-terminal 107 amino acids, and (2) an active disease model: direct immunization to mice with this recombinant protein. Results Immunoblotting revealed that 70% of patient sera reacted with the shorter recombinant protein of human laminin γ1 C-terminus. In the passive transfer model, rabbit IgG to the murine laminin γ1 C-terminus was deposited, without C3 deposition, at the epidermal basement membrane zone. In contrast, in the active disease model, direct immunofluorescence of mouse skin sections showed no deposition of either murine IgG or C3. Blister formation was not seen in either model both phenotypically and histopathologically. Conclusion In the two different mouse animal models for anti-laminin γ1 pemphigoid, although rabbit IgG to the recombinant laminin γ1 C-terminus bound to the epidermal basement membrane zone in passive transfer model, no obvious blister formation was seen. To reproduce skin lesions in mouse models for anti-laminin γ1 pemphigoid, further improvement should be needed. |
| Databáze: | OpenAIRE |
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