Immune checkpoint blockade has been widely presumed to rescue chronically stimulated, tumor-resident, exhausted T cells. However, researchers at Genentech (South San Francisco, CA, USA) found evidence for an alternate mechanism. Using single cell immune profiling, they observed that clonal expansion of effector-like T cells in patient tumors was reflected in normal adjacent tissue and peripheral blood. Further analysis suggested that, in patients responsive to anti-PDL1 therapy, intratumoral T cells are replenished with non-exhausted cells from outside the tumor. TD Wu et al., Nature. (2020).
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