These studies thus suggest first that induction of pancreatic inflammation results in intestinal dysbiosis and second that CXCR3+ T cell–sensitized pDCs driving AIP are being stimulated by TLR9 ligands derived from organisms in the intestinal microflora that gain entry into the pancreas via a compromised intestinal barrier. This evidence concerns the gene CXCR3 and autoimmune pancreatitis.