Glioblastoma (GBM) is the most common and aggressive form of primary brain cancer, with no improvements in the 5-year survival rate of 4.6% over the past three decades. T-cell-based immunotherapies such as immune-checkpoint inhibitors and chimeric antigen receptor T-cell therapy have had outstanding success as treatments for some cancers, and pose as new survival-prolonging treatments for GBM patients. Major challenges for T-cell-based immunotherapy of GBM and other solid cancers is T-cell infiltration into tumours, which is mediated by chemokine-chemokine receptor and integrin-adhesion molecule interactions. However, in GBM, the interactions that facilitate T-cell homing into tumours are unknown. Here, we have characterised the complete chemokine receptor and integrin expression profiles of endogenous GBM T-cells and chemokine expression profile of GBM-associated cells by single-cell RNA-sequencing. Subsequently, chemokine receptors and integrins were validated at the protein level to reveal enrichment of multiple migratory receptors in GBM-infiltrating T-cell populations relative to T-cells in matched patient peripheral blood. Complementary chemokine ligand expression was then investigated in GBM biopsies and GBM-derived primary cell-lines. Together, enriched expression of homing receptor-ligand pairings identified in this work implicate a role for these axes in mediating T-cell infiltration into GBM lesions. These findings may permit identification of migratory receptors that could be exploited to improve T-cell-based immunotherapy for GBM and possibly other solid tumours.