In triple-negative breast cancer (TNBC), stromal restriction of CD8+ T cells associates with poor clinical outcomes and lack of responsiveness to immune-checkpoint blockade (ICB). To identify mediators of T cell stromal restriction, we profiled murine breast tumors lacking the transcription factor Stat3, which is commonly hyperactive in breast cancers and promotes an immunosuppressive tumor microenvironment. Expression of the cytokine Chi3l1 was decreased in Stat3 /  tumors. CHI3L1 expression was elevated in human TNBCs and other solid tumors exhibiting T cell stromal restriction. Chi3l1 ablation in the polyoma virus middle T (PyMT) breast cancer model generated an anti-tumor immune response and delayed mammary tumor onset. These effectswere associated with increased T cell tumor infiltration and improved response to ICB. Mechanistically, Chi3l1 promoted neutrophil recruitment and neutrophil extracellular trap formation, which blocked T cell infiltration. Our findings provide insight into the mechanism underlying stromal restriction of CD8+ T cells and suggest that targeting Chi3l1 may promote anti-tumor immunity in various tumor types. Using an epithelial cell surface proteomic approach, we identified ectonucleotide pyrophosphatase/phosphodiesterase 1(ENPP1) as a functional regulator of the immune cold microenvironment.We generated a knock-in model of HER2D16 under the endogenous promoter to understand the role of Enpp1 in aggressive HER2 breast cancer. Knockdown of Enpp1 in HER2Delta16-derivedtumor cells resulted in decreased tumor growth, which correlated with increased T-cell infiltration. These findings suggest thatHER2Delta16-dependent Enpp1 activation associates with aggressive HER2 breast cancer through its immune modulatory function. Our study provides a better understanding of the mechanisms underlying HER2D16-mediated oncogenicity and highlights ENPP1 as a potential therapeutic target in aggressive HER2 breast cancer.