Figure 2.

Potential role of microbes and environmental triggers in CeD pathogenesis. Microbes that include both commensals and opportunistic pathogens may contribute to the development of CeD by influencing gluten peptide digestion, intestinal barrier function, epithelial cell stress, or IEL activation/upregulation through IL-15 regulation. Pathogenic bacteria, viruses, and non-gluten components of wheat, such as amylase-trypsin inhibitors (ATIs), may also induce DC maturation and proinflammatory cytokine production, modulating the induction of CD4+ T-cell responses.