The humanized SCID mouse model to study HLA class II-linked autoimmunity to desmoglein 3 in pemphigus vulgaris
| Autor: | Michael Hertl, T. RÄdisch, R. Riechers |
|---|---|
| Rok vydání: | 2002 |
| Předmět: |
Autoimmunity
Dermatology Mice SCID medicine.disease_cause Desmoglein Mice In vivo Immunopathology medicine Animals Humans education Autoimmune disease education.field_of_study biology Desmoglein 3 business.industry Pemphigus vulgaris HLA-DR Antigens medicine.disease Cadherins Disease Models Animal Immunoglobulin M Lymphocyte Transfusion Immunology Models Animal biology.protein Female Antibody business Pemphigus HLA-DRB1 Chains |
| Zdroj: | The British journal of dermatology. 146(2) |
| ISSN: | 0007-0963 |
| Popis: | Summary Background Pemphigus vulgaris (PV) is a severe autoimmmune skin disorder induced by antibodies against desmoglein (Dsg) 3 on epidermal keratinocytes. Objectives To establish an active animal model of PV to analyse the T-cell-regulated production of pathogenic antibodies in vivo. Methods Immunodeficient SCID mice were injected with peripheral blood lymphocytes (PBL) from an HLA-DRB1*0402/DQ8+ patient with PV or a DRB1*0402/DQ8+ healthy donor, with or without subsequent injections of human Dsg3 or preincubation of PBL with Dsg3. Results Human immunoglobulins (2·7–18·5 mg mL−1) were detected in all the mice after 8 weeks. Only one of 30 PBL-treated mice developed IgM against Dsg3 and showed intercellular IgM deposits in skin, nostrils and tongue. In contrast, in a previous study, 41% of SCID mice injected with PBL from patients with PV developed anti-Dsg3 antibodies in vivo. Conclusions Our inability to reproduce these findings may be due to the transfer of slightly lower numbers of PBL (20 × 106 vs. 25–30 × 106). |
| Databáze: | OpenAIRE |
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