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We have investigated the relationship between kinetic expression of CD45 on acinar cells during acute pancreatitis (AP) and the ability of these cells to produce tumour necrosis factor\u2010\u03b1 (TNF\u2010\u03b1) through mechanisms sensitive to the cellular redox state. Flow cytometric analysis showed a significant decrease in the constitutive expression of CD45 in acinar cells from six hours onwards after inducing AP by bile\u2010pancreatic duct obstruction (BPDO) in parallel with a significant increase in acinar TNF\u2010\u03b1 production. Changes in protein expression on the acinar cell surface preceded <jats:italic>CD45<\/jats:italic> mRNA down\u2010regulation, which was not found until 12 hours after BPDO. <jats:italic>N<\/jats:italic>\u2010Acetylcysteine treatment delayed and reduced the down\u2010regulation of CD45 expression induced by AP and prevented acinar cells from producing TNF\u2010\u03b1. Our results show that CD45 expression is down\u2010regulated in acinar cells during acute pancreatitis by redox\u2010sensitive mechanisms, and they support the notion that CD45 negatively controls the production of cytokines in pancreatic acinar cells. Copyright \u00a9 2006 Pathological Society of Great Britain and Ireland. 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