| First Author | Khare SD | Year | 1995 |
| Journal | J Exp Med | Volume | 182 |
| Issue | 4 | Pages | 1153-8 |
| PubMed ID | 7561688 | Mgi Jnum | J:110767 |
| Mgi Id | MGI:3641024 | Doi | 10.1084/jem.182.4.1153 |
| Citation | Khare SD, et al. (1995) Spontaneous inflammatory arthritis in HLA-B27 transgenic mice lacking beta 2-microglobulin: a model of human spondyloarthropathies. J Exp Med 182(4):1153-8 |
| abstractText | Human class I major histocompatibility complex allele HLA-B27 is associated with a group of human diseases called 'spondyloarthropathies.' Studies on transgenic rats expressing HLA-B27 and human beta 2-microglobulin have confirmed the role of HLA-B27 in disease pathogenesis. Here we report spontaneous inflammatory arthritis in HLA-B27 transgenic mice lacking beta 2-microglobulin (B27+ beta 2m-/-). In the absence of beta 2-microglobulin, B27+ beta 2m-/- animals do not express the HLA-B27 transgene on the cell surface and have a very low level of CD8+ T cells. Most of the B27+ beta 2m-/- male mice showed nail changes, hair loss, and swelling in paws, which leads to ankylosis. The symptoms occur only after the B27+ beta 2m-/- mice are transferred from the specific pathogen-free mouse colony. These results suggest that aberrant assembly, transport, and expression of the HLA-B27 molecule may predispose an individual for development of the disease when exposed to an appropriate environmental trigger. |
