There is accumulating evidence implicating the type I interferons (IFNs), including IFNα in the pathogenesis of type 1 diabetes. A recent study demonstrated treatment of 2-3 week old NOD mice with neutralizing antibody for the type I IFN receptor (IFNAR1) reduced and delayed the onset of diabetes. This suggests type I IFNs could be important in the initiation of diabetes. To test this directly we generated NOD mice deficient in the type I IFN receptor (NOD.IFNAR1) through backcrossing. These mice were genotyped for single nucleotide polymorphisms and were NOD genotype across the genome except for a 5.5Mb region on chromosome 16 that encompasses the IFNAR1 gene. We studied expression of type I IFN-induced genes in islets isolated from 2 week and 6 week-old NOD mice. Expression of type I IFN induced genes including Mx1, Ifit1 and Oas1a was elevated in NOD islets as early as 2 weeks of age, and expression was significantly reduced in NOD.IFNAR1 islets (p<0.0001). This suggests a contribution of type I IFN signalling within islets very early in NOD mice. Despite this NOD.IFNAR1 mice developed spontaneous diabetes and islet infiltration at a similar rate to NOD controls. To analyse the beta cell response to type I IFNs we quantitated the surface expression of MHC class I protein using flow cytometry. Class I protein expression increased as mice aged in both the NOD and NOD.IFNAR1 mice suggesting type I IFNs are dispensable for this process. However a deficiency of IFNγ receptors prevented this upregulation of MHC class I, suggesting that expression of MHC class I is primarily regulated by IFNγ in beta cells. The data demonstrate that despite the early responsiveness of islets to IFNα, type I IFN signalling is dispensable in development of diabetes, possibly due to overlapping effects of other cytokines including IFNγ.