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 wildtype 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 Tcell 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.
Interleukin-4 Deficiency Does Not Exacerbate Disease in NOD Mice
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Bo Wang, Antonio Gonzalez, Petter Höglund, Jonathan D Katz, Christophe Benoist, Diane Mathis; Interleukin-4 Deficiency Does Not Exacerbate Disease in NOD Mice. Diabetes 1 August 1998; 47 (8): 1207–1211. https://doi.org/10.2337/diab.47.8.1207
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