Interleukin-4 deficiency does not exacerbate disease in NOD mice.
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.[1]References
- Interleukin-4 deficiency does not exacerbate disease in NOD mice. Wang, B., Gonzalez, A., Höglund, P., Katz, J.D., Benoist, C., Mathis, D. Diabetes (1998) [Pubmed]
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