Abstract
Use of immune checkpoint inhibitors (ICIs) as cancer immunotherapy has advanced rapidly in the clinic; however, ICI initiation can also cause an unexpectedly rapid acceleration of cancer progression in some patients. Here, we used a murine syngeneic melanoma model to conduct mechanistic analysis of cancer-associated fibroblast (CAF) function in cancer progression in the context of immunotherapy. We found that after ICI treatment CAFs acquire inflammatory properties, which can promote tumor progression. Mechanistically, we show that T-cell-derived interferon-γ (IFN-γ) stimulates production of tumor necrosis factor-α (TNF-α) by macrophages, facilitating CAF conversion to inflammatory CAFs. Our findings suggest that CAF/immune cell crosstalk plays an essential role in ICI-associated tumor progression.
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