IFNγ is a central node in cancer immune equilibrium

The anti-tumor effects of IFNγ are well-known as IFNγ binding to tumor cells increases antigen presentation and can cause cytostatic growth defects. Indeed, the inability of tumors to respond to IFNγ often renders tumors resistant to checkpoint blockade and other immunotherapies reliant on direct T cell cytotoxicity. We demonstrate through RNA-sequencing that IFNgR1-/- and STAT1-/- tumors are defective in their response to IFNγ compared to wild-type tumors. Wild-type, STAT1-/-, and IFNgR1-/- B16-Nectin1+ cells were cultured in vitro for 24 hours with 0 or 100 ng/ml IFNγ. Total RNA was extracted from cells of biological triplicates.