| First Author | Tsunoda K | Year | 2002 |
| Journal | Eur J Immunol | Volume | 32 |
| Issue | 3 | Pages | 627-33 |
| PubMed ID | 11857336 | Mgi Jnum | J:115362 |
| Mgi Id | MGI:3691499 | Doi | 10.1002/1521-4141(200203)32:3<627::AID-IMMU627>3.0.CO;2-1 |
| Citation | Tsunoda K, et al. (2002) Pathogenic autoantibody production requires loss of tolerance against desmoglein 3 in both T and B cells in experimental pemphigus vulgaris. Eur J Immunol 32(3):627-33 |
| abstractText | Mechanisms of tolerance break against desmoglein 3 (Dsg3) in patients with pemphigus vulgaris (PV) producing pathogenic anti-Dsg3 IgG autoantibodies are unclear. In this study, using a novel PV mouse model involving Dsg3 knockout mice, we investigated the mechanisms leading to production of autoantibodies against Dsg3. Adoptive transfer of Dsg3(-/-) splenocytes immunized with recombinant mouse Dsg3 to Rag2(-/-) recipient mice expressing Dsg3 resulted in the stable production of anti-Dsg3 IgG and development of PV phenotypes including oral erosions with suprabasilar acantholysis. When purified T and B cells from Dsg3(-/-), Dsg3(+/-) or Dsg3(+/+) mice were mixed with various combinations and transferred to Rag2(-/-) mice, pathogenic anti-Dsg3 IgG production was observed only with a combination of Dsg3(-/-) T and Dsg3(-/-) B cells but not with the other combinations. These results suggest that loss of tolerance against Dsg3 in both B and T cells is important for the development of autoimmune state of PV. |
