That such CCL25-mediated pDC chemoattraction originating from a cDC–T cell interaction in the early induction phase of experimental AIP (as well as a pDC–T cell interaction in the mature phase of experimental AIP) occurs in vivo and is essential to the progression of the pancreatic inflammation was shown by the fact that administration of anti-CCL25 Ab at the time of poly(I:C) administration prevents production of IFN-α and IL-33 and the development of AIP. This evidence concerns the gene IL33 and autoimmune pancreatitis.