Our findings indicate that genes that show increased expression in human IBD colon biopsies, including those with mutations that have been linked to an increased risk of Crohn’s disease and/or ulcerative colitis, such as NOD2, IL23R, IL21 and IFNG11, are differentially abundant in the LPLs from H. hepaticus-infected mice with T cell-specific deletion of Prdm1, Maf or both transcription factors, suggesting that these mouse models may reflect different pathobiological mechanisms relevant in human IBD. The gene discussed is NOD2; the disease is inflammatory bowel disease.