The analysis of pathophysiology of autoimmune bullous diseases by using retrovirus vector

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Pemphigus vulgaris (PV) is an autoimmune bullous disease with circulating IgG autoantibodies against desmogleins (Dsg). We recently established Dsg3-specific T cell clones that induced PV phenotype and isolated cDNA clones of their T cell receptors (TCR). Herein, we retrovirally transduced wild type CD4^+ T cells with these TCR cDNAs (rvDsg3 T cells) to clarify their pathogenic roles for antigen-specific autoimmune processes in skin. When rvDsg3 T cells were transferred with Dsg3^<-/-> B cells into Rag2^<-/-> mice, the recipient mice neither showed clinical PV phenotype, anti-Dsg3 IgG production, nor histological evidence for acantholysis, but instead developed scaly and erythematous skin lesions. Histology revealed interface dermatitis only in skin, mucous membranes and esophagus, where Dsg3 was expressed.