| First Author | Wang B | Year | 1998 |
| Journal | Diabetes | Volume | 47 |
| Issue | 8 | Pages | 1207-11 |
| PubMed ID | 9703318 | Mgi Jnum | J:85924 |
| Mgi Id | MGI:2677558 | Doi | 10.2337/diab.47.8.1207 |
| Citation | Wang B, et al. (1998) Interleukin-4 deficiency does not exacerbate disease in NOD mice. Diabetes 47(8):1207-11 |
| abstractText | To investigate the role of interleukin (IL)-4 in the regulation of autoimmune diabetes, we crossed the IL-4 knock-out mutation onto the NOD genetic background. This experiment was accelerated by typing for microsatellites linked to known diabetes susceptibility (Idd) loci, and included a control backcross of the wild-type 129/SvJ-derived IL-4 gene, the original target locus. We also crossed the mutation into the BDC2.5 transgenic line, a diabetes model that carries the rearranged T-cell receptor genes from a diabetogenic T-cell clone. The IL-4-null mutation did not accelerate or intensify insulitis in regular NOD mice or in the BDC2.5 transgenic model; it also had no effect on the timing or frequency of the transition to overt diabetes. These data indicate that IL-4 plays no required role in controlling the aggressiveness of murine diabetes. |
