Britya Ghosh

[Leukemia] Ex vivo treatment of cells from acute myeloid leukemia (AML) mice and AML patients with bromodomain and extra-terminal domain (BET) inhibitors reversed CD8+ T cell exhaustion by restoring proliferative capacity and expansion of the more functional precursor-exhausted T cells.

[Nature Communications] The authors reported that specific deletion of IFNγR in CD8 T cells promoted tumor control in a mouse model of melanoma, and provide evidence of a negative feedback loop whereby IFNγ depletes stem-like T cells to restrict anti-tumor immunity.

[Nature Immunology] Selectively targeting YTHDF2 in tumor-associated macrophages (TAMs) using a Toll-like receptor 9 agonist-conjugated small interfering RNA reprogrammed TAMs toward an antitumoral phenotype, restrained tumor growth, and enhanced the efficacy of PD-L1 antibody therapy.