SRA

Colonies of non-obese diabetic (NOD) mice have different susceptibilities to developing type I diabetes (T1D). In our colony, a degree of resistance to T1D development is dependent on maternal immune deficiencies that induce shifts in the maternal microbiome composition. This altered microbiome is vertically transmitted to offspring, and the resulting disease protection has been linked to upregulated transcription of numerous immune pathways along the intestinal tract during early life. In the transcriptomics dataset, we compared the mRNA content of ileal (small bowel, SB) and colonic (large bowel, LB) tissue from disease resistant vs susceptible pups at weaning, where the upregulated transcriptional pathways are evident in the SB tissue of pups from IgA-deficient dams. The genomic 16S sequencing dataset compares the microbiome compositions of IgA-deficient vs -sufficient dams, as well as those of their offspring at 3 weeks and 12 weeks of age.