Studies in humans show that MHC class II expression is absent from small intestinal crypts under normal physiologic conditions but is upregulated in specimens obtained from patients with active IBD, celiac disease, and graft vs. host disease.34–38 Exposure to inflammatory antigens, such as gliadin in celiac disease, has also been shown to cause the upregulation of cell surface MHC class II and activate effector CD4+ T cells. This evidence concerns the gene CD4 and inflammatory bowel disease.