| First Author | Oble DA | Year | 2005 |
| Journal | J Invest Dermatol | Volume | 124 |
| Issue | 1 | Pages | 151-9 |
| PubMed ID | 15654969 | Mgi Jnum | J:95380 |
| Mgi Id | MGI:3525924 | Doi | 10.1111/j.0022-202X.2004.23565.x |
| Citation | Oble DA, et al. (2005) A novel T cell receptor transgenic animal model of seborrheic dermatitis-like skin disease. J Invest Dermatol 124(1):151-9 |
| abstractText | We have characterized a novel animal model of the common inflammatory skin disease seborrheic dermatitis (SD) that involves the expression of the self-specific 2C transgenic T cell receptor on the DBA/2 genetic background. Opportunistic fungal pathogens are present in the primary histological lesions and severe disease can be mitigated by the administration of fluconazole, demonstrating a role for infection in disease pathogenesis. Spontaneous disease convalescence occurs at 70-90 d of age and is preceded by an expansion of CD4(+) T cells that partially restores the T cell lymphopenia that occurs in these animals. The adoptive transfer of syngeneic CD4(+) T cells into pre-diseased DBA/2 2C mice completely abrogates the development of cutaneous disease. The pattern of disease inheritance in DBA/2 backcrosses suggests that one, or a closely linked group of genes, may control disease penetrance. Bone marrow reconstitution experiments demonstrated that the DBA/2 susceptibility factor(s) governing disease penetrance is likely non-hematopoietic since bone marrow from disease-resistant 2C mice can adoptively transfer the full disease phenotype to non-transgenic DBA/2 animals. This model implicates fungal organisms and CD4(+) T cell lymphopenia in the development of a SD-like condition and, as such, may mimic the development of SD in acquired immunodeficiency syndrome. |
