Primary brain tumors, such as glioblastoma (GBM), have been remarkably resistant to immunotherapy, even though pre-clinical models suggest effectiveness. To understand this better in patients, we took advantage of our recent neoadjuvant treatment paradigm to map the infiltrating immune cell landscape of GBM and how this is altered following PD-1 checkpoint blockade using high dimensional proteomics, single cell transcriptomics, and quantitative multiplex immunofluorescence. Neoadjuvant PD-1 blockade increased T cell infiltration and proportion of a progenitor exhausted population of T cells found within the tumor. We identified an early activated and clonally expanded CD8+ T cell cluster whose TCR overlapped with a CD8+ PBMC population. Distinct changes were also observed in conventional type 1 dendritic cells that may facilitate T cell recruitment. Macrophages and monocytes still constituted the majority of infiltrating immune cells, even after anti-PD-1 therapy. Interferon-mediated changes in the myeloid population were consistently observed following PD-1 blockade; these also mediated an increase in chemotactic factors that recruit T cells. However, sustained high expression of T-cell-suppressive checkpoints in these myeloid cells continued to prevent the optimal activation of the tumor infiltrating T cells. Therefore, future immunotherapeutic strategies may need to incorporate the targeting of these cells for clinical benefit.