Chronic pancreatitis is a disease whose pathomechanism has not yet been fully explained. Some progress has been made in recent years, however, mainly due to the identification and description of pancreatic stellate cells (PSCs). In 1998 Bachem observed that the vitamin A-storing cells present in the pancreas, when subjected to activation, transformed into myofibroblasts capable of producing collagens I and II and fibronectin, which contributes to fibrosis in chronic pancreatitis. The development of chronic pancreatitis also seems likely to be affected by the cytokines, among other things, as a result of repeated PSC activation. The current literature provides more and more data suggesting that cytokines play an important role in the regulation of inflammation and fibrosis in CP. A major role in the pathogenesis of chronic pancreatitis is attributed to interleukin 1, 6, 10, tumour necrosis factor a (TNF-a) and transforming growth factor b1 (TGF-b1). All these factors have pro- and anti-inflammatory effects, and act simultaneously. Their effects on PSCs can be synergistic, antagonistic or complementary. Further comprehensive studies are needed to determine precisely the role of the individual cytokines and PSCs, as well as their relationships. However, the present state of our knowledge suggests that repeated episodes of AP and thus exposure to increased cytokine secretion may contribute to persistent chronic activation of PSCs, resulting in pancreatic fibrosis and chronic pancreatitis.