The pathogenesis of chronic pancreatitis (CP) is still controversial. None of the proposed models has been able to provide a convincing link between the known etiological factors - alcohol abuse, metabolic disturbances, congenital or acquired obstruction of the duct system - and the complex morphological and pathophysiological aspects of the disease. Molecular and cell biology research during the last years, however, has elucidated that a dysregulated immune response, together with an active involvement of pancreatic parenchymal cells, contributes to tissue destruction, fibrosis and remodeling in CP. Infiltration of the pancreas by particular subsets of immune effector cells, aberrant and enhanced expression of MHC molecules, and overexpression of growth factors and their receptors have all recently been found to play a role in CP. In addition, genetic analysis has led to the discovery of genes that predispose their carriers to the development of the disease, and has shed new light on the relation between CP and pancreatic cancer.