c-Maf-dependent regulatory T cells mediate immunological tolerance to a gut pathobiont

Both microbial and host genetic factors contribute to the pathogenesis of autoimmune disease. Accumulating evidence suggests that microbial species that potentiate chronic inflammation, as in inflammatory bowel disease (IBD), often also colonize healthy individuals. These microbes, including the Helicobacter species, have the propensity to induce pathogenic T cells and are collectively referred to as pathobionts. However, an understanding of how such T cells are constrained in healthy individuals is lacking. For this study we wanted to compare the transcriptomes of H. hepaticus-specific T effector cells from mice that were IL-10-deficient to those that were Maf-deficient in the Treg compartment to determine if they share an inflammatory signature. We also compared Maf -sufficient and -deficient polyclonal iTreg to determine molecular targets of the TF c-Maf. 12 samples with 2 replicates each