Remodelling of the immune landscape by IFNγ counteracts IFNγ-dependent tumour escape in mouse tumour models.

ABSTRACT: Loss of IFNγ-sensitivity by tumours is thought to be a mechanism enabling evasion, but recent studies suggest that IFNγ-resistant tumours can be sensitised for immunotherapy, yet the underlying mechanism remains unclear. Here, we show that IFNγ receptor-deficient B16-F10 mouse melanoma tumours are controlled as efficiently as WT tumours despite their lower MHC class I expression. Mechanistically, IFNγ receptor deletion in B16-F10 tumours increases IFNγ availability, triggering a remodelling of the immune landscape characterised by inflammatory monocyte infiltration and the generation of 'mono-macs'. This altered myeloid compartment synergises with an increase in antigen-specific CD8⁺ T cells to promote anti-tumour immunity against IFNγ receptor-deficient tumours, with such an im

SUBMITTER: Lau VWC 

PROVIDER: S-EPMC11696141 | biostudies-literature | 2025 Jan

REPOSITORIES: biostudies-literature