Relating to the necessity for (and advantage of) this switch in the DC type driving AIP, we demonstrated with in vitro studies that pDCs produce large amounts of type I IFNs upon ligand stimulation and CXCR3+ T cell interaction; similarly, the amount of CXCR3+ T cell–derived CCL25 necessary for further pDC recruitment was much greater in the presence of pDCs than that produced by the same T cell population in the presence of cDCs. The gene discussed is CXCR3; the disease is autoimmune pancreatitis.