Severe acute pancreatitis (SAP) presents with a fulminant clinical course, and immune imbalance serves as a core pathophysiological process throughout disease progression. Focusing on the dynamic evolution of SAP, this review elaborates the molecular mechanisms by which acinar cell injury triggers the immune cascade, delineates the functional heterogeneity of innate and adaptive immune cells, cytokine regulatory networks, and the mechanisms of distant organ injury mediated by the gut lymphatic pathway, and systematically summarizes research advances in core diagnostic immune biomarkers categorized into proinflammatory cytokines, immune cell-associated indicators, endothelial injury markers and omics-derived molecules, thereby providing theoretical evidence for severity stratification and mechanistic investigation of SAP.