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Aims: Excessive stroma and cancer-associated fibroblasts (CAFs) enhance cancer progression through the interaction with cancer cells. However, understanding of immune microenvironment manipulated by stroma is still insufficient. We aimed to uncover the underlying mechanism and the significance of stromal remodeling in cancer immunotherapy.Methods: We examined the significance of stroma amount, PDGF ligands and receptors in GC tissues. Reverse-phase protein array (RPPA) analysis and RNA sequencing were used to examine the reaction by PDGF ligands in human CAFs. Fibrotic tumor mouse model was developed by serial transplantation of mouse GC cell line (GAN-KP cells) from genetically engineering GC mouse model to address the role of CAFs in immune microenvironment, and was used to validate the effect of combined immunotherapy. Single-cell RNA-sequencing (scRNA-seq) and spatial transcriptomics were performed to investigate the effect of PDGFRa/b dual blockade on stromal remodeling. Results: PDGFC and D expression were significantly associated with poor prognosis of GC patients and PDGFRb was dominantly expressed in diffuse-type GC (DGC) stroma. CAFs stimulated by PDGF ligands remarkably increased the growth and the expression of CXCL1, 3, 5 and 8 involving polymorphonucler myeloid-derived suppressor cells (PMN-MDSC) recruitment. In addition, serial transplanted fibrotic tumors exhibited decrease of tumor infiltrating lymphocytes, PMN-MDSC accumulation and resistance to anti-PD-1 antibody. PDGFRa/b dual blockade improved the immunosuppressive microenvironment through stromal remodeling and demonstrated the synergistic effect with anti-PD-1 antibody on fibrotic tumors. Conclusions: These findings highlight the evidence of stromal remodeling for immune reactivation in fibrotic cancer exhibiting immune checkpoint inhibitor resistance, leading to rational design of combined immunotherapy.