Transgenic mice are viable, fertile, normal in size, normoglycemic and do not display any gross physical or behavioral abnormalities. High levels of the transgene are expressed on B cells, but not on T cells. At 30 weeks of age transgenic mice are diabetes resistant and insulitis was significantly reduced when compared with wildtype NOD controls. When compared to wildtype NOD controls, the circulating B cells in congenic NOD transgenic mice is 2-3 fold lower in 2 week old mice and 10 fold lower in 5-6 week old mice and persists throughout life. Significantly reduced percentage of B cells were found in the spleen and bone marrow. Analysis of bone marrow shows the more mature B cell subsets (B220+, IgM+) are affected. Elisa tests indicate reduced circulating levels of all Ig types, Ighm (formerly Igh-6), Igh-3 (IgG2b), and Ighg1 (IgG1) in the serum of transgenic mice. MHC class II expression of splenic B cells was significantly increased by more than 2 fold, indicating features of an activated B cell phenotype, in NOD-H2g7 transgenic mice when compared to NOD wildtype and NOD.-H2b transgenic mice.
In 2008, a spontaneous mutation to dystonia (Dst) was observed in this colony and may be segregating in cryopreserved stock.
This strain may be used to study autoreactive T cell activation and B cell deletion and the role of B7 costimulatory molecules in autoimmunity, specifically Type 1 Diabetes.
