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. 2022 Mar 23;24(10):1647–1657. doi: 10.1093/neuonc/noac055

Fig. 1.

Fig. 1

T cells shape glioma evolution. Glioma cells recruit T cells into the tumor microenvironment (TME) through the elaboration of chemokines. In addition, T cells produce paracrine factors that can act on other cells in the TME (eg, microglia) to increase tumor growth (“cooption”). Pro-tumoral regulatory T cells (Tregs) can also function to increase glioma growth (“equilibrium”), while cytotoxic T lymphocytes (CTLs) lyse tumor cells by secreting perforin (PFN) and granzyme B (GZMB) or by direct cell-to-cell interaction (“elimination”). Other CTLs can adopt an “exhausted” phenotype or become inactivated by glioma cells through the expression of immune checkpoint proteins. In response to extrinsic or intrinsic pressures, the balance of pro- and anti-tumoral T cells can shift to favor CTLs, resulting in glioma elimination. Created with BioRender.