| First Author | Lund T | Year | 1990 |
| Journal | J Autoimmun | Volume | 3 |
| Issue | 3 | Pages | 289-98 |
| PubMed ID | 1975742 | Mgi Jnum | J:10713 |
| Mgi Id | MGI:59159 | Doi | 10.1016/0896-8411(90)90147-k |
| Citation | Lund T, et al. (1990) Restriction fragment length polymorphisms in the major histocompatibility complex of the non-obese diabetic mouse. J Autoimmun 3(3):289-98 |
| abstractText | The inbred non-obese diabetic (NOD) mouse is a spontaneous model for insulin-dependent diabetes mellitus (IDDM). As in man and BB rats, IDDM in the NOD mouse has an autoimmune aetiology. The disease is controlled by several genes, one of which, Idd-1, has been mapped to the major histocompatibility complex (MHC) on chromosome 17. However, Idd-1 has not yet been identified. To facilitate the identification of Idd-1 we have further analysed the MHC region for restriction fragment length polymorphisms and we find that the NOD mouse has a distinct haplotype: H-2K1nod Kd A beta nod A alpha d E beta nod TNF-alpha beta. In addition, the NOD mouse shows some similarities with the H-2b haplotype in the Q region, in that either the Q7 or the Q9 gene seems to be like that in the b-haplotype and that the Qa2 antigen is expressed, while other parts of this region are distinct from the b- as well as the d- haplotype. In contrast, the sister strain, the non-obese normal (NON) mouse, derived from the same cataract-prone line of mice as the NOD mouse, has an MHC Class I region indistinguishable from the b-haplotype, but the MHC Class II region is distinct from the NOD mouse as well as the b-, d- and k-haplotype. |
