pancreatic cancer is characterized by a profoundly immunosuppressive tumor microenvironment, rendering it a prototypical“cold tumor”and limiting the efficacy of immune checkpoint inhibitors (ICIs) as monotherapy. In recent years, various combination strategies have been proposed to enhance the therapeutic response to ICIs, including their integration with chemotherapy, radiotherapy, targeted therapy, oncolytic viruses, STING agonists, personalized vaccines, and chimeric antigen receptor (CAR) T-cell therapies. These combinatorial approaches aim to induce immunogenic cell death, activate interferon signaling pathways, remodel the tumor microenvironment, and enhance T cell function, thereby increasing the immunogenicity of pancreatic cancer. Although preliminary studies have shown that such combinations can yield clinical benefits, challenges remain complex, including increased immune-related toxicity, high interpatient heterogeneity, the lack of predictive biomarkers, and complex mechanisms of resistance. Future efforts should focus on refining patient selection, elucidating underlying biological mechanisms, and conducting robust clinical trials to facilitate the transition of immunotherapy for pancreatic cancer from experimental exploration to standardized clinical application, particularly in advanced-stage and adjuvant treatment settings.