| First Author | Khare SD | Year | 2001 |
| Journal | Clin Immunol | Volume | 98 |
| Issue | 3 | Pages | 364-9 |
| PubMed ID | 11237560 | Mgi Jnum | J:115586 |
| Mgi Id | MGI:3691966 | Doi | 10.1006/clim.2000.4984 |
| Citation | Khare SD, et al. (2001) Spontaneous inflammatory disease in HLA-B27 transgenic mice does not require transporter of antigenic peptides. Clin Immunol 98(3):364-9 |
| abstractText | HLA-B27 is strongly linked with a group of human diseases called spondyloarthropathies. Even though HLA-B27 as an MHC class I molecule would be expected to present endogenously processed peptides such as cytosolic or viral proteins, many of the B27-linked diseases begin after an infection with an enterobacteria, an exogenous antigen. In our previous studies, we have described development of spontaneous inflammatory disease in HLA-B27 transgenic mice expressing beta(2)m free heavy chains on the cell surface. In order to address the role of endogenous versus exogenous antigens and a role for Tap genes in the development of spontaneous diseases, mice lacking Tap-1 (knockout) were mated to HLA-B27/human beta(2)m transgenic mice. B27(+)/human beta(2)m(+) double-transgenic mice (without mouse beta(2)m) lacking the Tap-1 gene developed spontaneous inflammatory disease similar to wild-type Tap-1 gene-expressing counterparts. Our data demonstrate that peptide transporters (Tap) were not involved in the development of spontaneous inflammatory disease in B27(+)/human beta(2)m transgenic animals. |
