CCR2+HSCs cross-prime endogenous T lymphocytes. a Either HSCs, CCR2+HSCs, or CCR2−HSCs isolated from DsRed+ mice were stereotactically injected into tumors of glioma-bearing mice. DsRed+ cells were then observed in draining lymph nodes 1 week post transfer, and relative amounts of DsRed+ cells between groups was compared, CCR2+HSCs vs. CCR2−HSCs (*p = 0.021, Mann–Whitney, n = 5 mice per group). b Either HSCs, CCR2+HSCs, or CCR2−HSCs were isolated from DsRed+ mice, then were stereotactically injected directly into tumors of glioma- or medulloblastoma-bearing mice followed by systemic administration of PD-1. Three weeks post transfer, draining lymph nodes were harvested and T-cells were isolated from the lymph nodes using magnetic bead isolation. These T-cells were then used as effector cells against tumor cell targets in a co-culture assay. This was conducted in KR158B glioma-bearing mice, and Ptc medulloblastoma-bearing mice, and IFNγ secretion was measured after the co-culture. T cells harvested from b KR158B glioma-bearing mice that received CCR2+HSCs secreted an average of 1549.99 ± 212.621 pg/ml IFNγ, which is significantly more that T-cells derived from mice that received CCR2−HSCs that contained 522.183 ± 87.32 pg/ml IFNγ (**p = 0.0111, two-tailed t-test). c T cells harvested from Ptc medulloblastoma-bearing mice that received CCR2+HSCs secreted an average of 972.2 ± 110.6 pg/ml IFNγ, which is significantly more that T-cells derived from mice that received CCR2−HSCs that contained 132.6 ± 20.74 pg/ml IFNγ (***p = 0.0017, two-tailed t-test). All error bars represent s.e.m.