Acquired resistance to PD-L1 inhibition is associated with an enhanced type I IFN-stimulated secretory program in tumor cells
Abstract
Background: Interferon (IFN) pathway activation in tumors can have dual, sometimes opposing, influences on immune responses. Therapeutic inhibition of programmed cell death ligand (PD-L1)-a treatment that reverses PD-1-mediated suppression of tumor-killing T-cells-is linked to alterations in IFN signaling; however, less is known about the role of IFNs after treatment resistance. Since IFN-regulated intracellular signaling can control extracellular secretory programs in tumors to modulate immunity, we examined the consequences of PD-L1 blockade on IFNrelated secretory changes in preclinical models of acquired resistance.
Domains
Cancer| Origin | Files produced by the author(s) |
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