Pancreatic ductal adenocarcinoma (PDA) is a lethal disease killing about 7000 people in the United Kingdom every year. PDA is resistant to conventional therapy. A hallmark of PDA is the abundance of desmoplastic stroma, which is thought to originate by activation of pancreatic stellate cells (PSC). Unfortunately, little is know about the precise role of PSC in the physiology of the pancreas. In this proposal I will investigate the function of the pancreatic stellate cell in health and during tumour development using a murine model of PDA. I hypothesize, that PSC function as antigen-presenting cells surveying the microenvironment for tissue damage. I postulate, that PSC induce repair processes as well as immunosuppressive responses by means of retinoic acid signalling (PSC are a major vitamin A storage) and the secretion of TGFbeta. This anti-inflammatory program may serve to prevent the autoimmune destruction of the pancreas, an organ indispensable for survival. However, during cancer development this default program may be detrimental as it inhibits the mounting of a proper anti-tumour response.