| First Author | Rietz C | Year | 2003 |
| Journal | Scand J Immunol | Volume | 57 |
| Issue | 4 | Pages | 342-9 |
| PubMed ID | 12662297 | Mgi Jnum | J:131889 |
| Mgi Id | MGI:3774787 | Doi | 10.1046/j.1365-3083.2003.01244.x |
| Citation | Rietz C, et al. (2003) Overexpression of bcl-2 in T cells affects insulitis in the nonobese diabetic mouse. Scand J Immunol 57(4):342-9 |
| abstractText | The nonobese diabetic (NOD) mouse is a useful model for human autoimmune diabetes. The gene for the anti-apoptotic protein Bcl-2 has previously been suggested as a probable susceptibility candidate for the NOD mouse disease. In this study, we investigated how overexpression of Bcl-2 in lymphocytes might affect insulitis in NOD mice. A bcl-2 transgene expressed constitutively under the SV40-promoter and the 5'Igh enhancer, Emu, was bred onto NOD background. Two bcl-2 transgenic NOD strains were produced and analysed, one with overexpression of Bcl-2 on only B cells and the other with overexpression of Bcl-2 on both B and T cells. Subsequent to verification of expression pattern and functionality of the transgene, insulitis intensity was investigated in different backcross generations of the two transgenic strains. Overexpression of Bcl-2 on both B and T cells leads to a statistically significant protection of the mice from insulitis compared with normal littermates. Overexpression of Bcl-2 on only B cells, on the other hand, does not have any statistically significant effect on insulitis. Possible mechanisms for the effect of Bcl-2 on insulitis in NOD mice are discussed. |
