<p>Macrophages are among the most abundant immune cells in solid tumors, yet how macrophage lineage and spatial organization shape antitumor immunity remains unclear. Here we uncovered a division of labor between tissue-resident CD206^hi and CD206^lo interstitial macrophage (IM) subsets and <i>Ly6c2</i>⁺<i>Fn1</i>⁺<i>Vcan</i>⁺ recruited macrophages (recMacs) in lung cancer. Using single-cell and spatial transcriptomics, we identified chemokine-expressing IM subsets with opposing functions. <i>Cxcl13</i>⁺CD206^hi IMs, <i>Cxcl9</i>⁺CD206^hi IMs and <i>Cxcl10</i>⁺CD206^hi IMs positioned along bronchovascular regions drove tertiary lymphoid structure formation, lymphocyte recruitment and tumor control, whereas <i>Ccl2</i>⁺ IMs, localized within tumor regions, recruited protumorigenic <i>Ly6c2</i>⁺<i>Fn1</i>⁺<i>Vcan</i>^<i>+</i> recMacs. In addition, Ly6C⁺CD11b⁺ monocyte-derived dendritic cells (moDCs) functioned as immunosuppressive antigen-presenting cells in tumor-draining lymph nodes. During cancer vaccination, CCR5 blockade with maraviroc selectively inhibited antigen-bearing moDC migration, enhancing dendritic cell-mediated antitumor immunity. These findings showed how macrophage lineage and spatial compartmentalization govern tumor immunity and identified strategies to preserve protective IM functions, while disrupting macrophage-driven immunosuppression.</p>