Artigo Acesso aberto Revisado por pares

Pathogenic autoantibody production requires loss of tolerance against desmoglein 3 in both T and B cells in experimental pemphigus vulgaris

2002; Wiley; Volume: 32; Issue: 3 Linguagem: Inglês

10.1002/1521-4141(200203)32

ISSN

1521-4141

Autores

Kazuyuki Tsunoda, Takayuki Ota, Harumi Suzuki, Manabu Ohyama, Tetsuo Nagai, Takeji Nishikawa, Masayuki Amagai, Shigeo Koyasu,

Tópico(s)

Coagulation, Bradykinin, Polyphosphates, and Angioedema

Resumo

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.

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