T-cell dysfunction in the glioblastoma microenvironment is mediated by myeloid cells releasing interleukin-10.

In both CD8 + and CD4 + populations, a highly significant reduction in the number of cells within the exhausted T cell population was observed, suggesting that treatment with JAK-inhibitors could be a potential therapeutic option to boost T cell activation by reducing immunosuppressive programs in both myeloid and glial cells, Fig. 7e, f .

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