ReviewFrontiers in immunology2026
Tumor-intrinsic execution of interferon-γ-associated immunity in bladder cancer: checkpoints in signaling, recruitment, and recognition.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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4 authors.
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Abstract
Interferon-γ (IFN-γ) is a central mediator of antitumor immunity in bladder cancer, but an IFN-γ-rich tumor microenvironment does not necessarily translate into tumor control. Tissue-level inflammatory signatures capture overall immune activity and cannot determine whether malignant urothelial cells remain responsive to immune-derived IFN-γ or preserve the downstream functions required for immune elimination. This Mini Review examines tumor-intrinsic IFN-γ-associated immunity at three functional checkpoints: proximal IFN-γ sensing and signal transduction, chemokine-mediated effector-cell recruitment, and antigen-presentation-dependent tumor recognition. Bladder cancer models show that IFNGR-JAK-STAT1 responsiveness can be lost or attenuated, while separate tumor-intrinsic mechanisms can restrict CXCL9/CXCL10-dependent T-cell recruitment without a demonstrated proximal signaling defect. Antigen presentation forms a further checkpoint, with HLA-I and antigen-processing machinery altered through transcriptional, treatment-associated, and post-translational mechanisms. These mechanisms do not constitute a single linear IFN-γ resistance pathway. They instead mark distinct points at which inflammatory pressure can become uncoupled from tumor elimination. IFN-γ-responsive programs are also shaped by treatment context and signaling duration, as illustrated by CIITA/MHC-II biology and prolonged interferon signaling. Resolving these processes at malignant-cell, spatial, and longitudinal levels may improve the interpretation of BCG and checkpoint-blockade resistance and support more selective combination strategies.
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