Despite the clinical success of standard of care immunotherapies targeting PD-1/L1 by immune checkpoint blockade (ICB), almost two thirds of melanoma patients fail to respond. This disparity in clinical efficacy highlights the need to explore alternative targets for immunotherapy-resistant melanoma. We have previously demonstrated that inhibiting the immune checkpoint P-selectin glycoprotein ligand-1 (PSGL-1) by ICB improves tumor control in preclinical melanoma models, but there is a need to better understand how targeting PSGL-1 reshapes the tumor immune microenvironment (TME) in therapy-resistant melanoma. Here, we tested the hypothesis that PSGL-1 immune checkpoint expression on antigen presenting (APC) myeloid cells alters immune cells in the melanoma tumor microenvironment. To test this, we performed spectral flow cytometry to characterize D4M-3A melanoma tumor-infiltrating immune cells in wildtype (WT) or Selplg^-/- (KO) mice, and we found that KO mice had increased numbers of APCs with higher MHC-II expression. Additionally, we observed increased effector T cell responses in KO tumor-bearing mice, leading to improved tumor control. To assess the myeloid APC-specific contribution, we generated Selplg^fl/fl x CD11c-Cre (cKO) mice to delete PSGL-1 in myeloid cells and challenged them with D4M-3A melanoma. We show that in cKO mice, PSGL-1 expression was deleted across most DCs and macrophages in the TME, and cKO hosts had improved tumor control compared to WT mice. Furthermore, the numbers and function of tumor-infiltrating CD8+ T cells was improved in cKO mice, as evidenced by the increased stem-like progenitor exhausted (TXp) and effector-like intermediate exhausted (TXi) CD8 T cell subsets. Our data shows that PSGL-1 expression on myeloid cells is an inhibitory pathway that reshapes the immunosuppressive TME, and inhibiting this pathway may help reinvigorate immune responses against tumors.