Selective suppression of melanoma lacking ifn-γ pathway by jak inhibition depends on t cells and host tnf signaling

HIGHLIGHTS

SUMMARY

    Given the indispensable role of tumor-infiltrating T_cells (TILs) in ICBs, little is known about how tumorintrinsic loss of IFN-γ signaling (IFNγR1KO) impacts TILs. JAK1/2 inhibition with Ruxolitinib selectively suppresses the growth of IFNγR1KO but not scrambled control melanomas, depending on T_cells and host TNF. ICBs, by blocking immune checkpoints (namely, CTLA-4, PD-1, and PD-L1) hijacked by tumor cells to evade immunosurveillance, enhance the effector function (e_g, IFN-γ production)15,16 and decrease the abundance of immunosuppressive FoxP3+ regulatory T_cells (Treg) in TILs17, leading to tumor rejection. Subsequently . . .

     

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