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Area of Science:

  • Oncology
  • Immunology
  • Translational Research

Background:

  • Immune checkpoint blockade (ICB) offers a promising treatment for urothelial bladder cancer (UC), but limited response rates necessitate further investigation.
  • Systemic inflammation, indicated by elevated C-reactive protein (CRP), is linked to poorer clinical outcomes in UC patients.
  • Macrophages play a critical role in shaping the tumor microenvironment (TME) and influencing treatment response.

Purpose of the Study:

  • To investigate the association between systemic inflammation markers (IL-6, CRP) and tumor macrophage infiltration in UC.
  • To identify specific macrophage subsets within the TME that correlate with systemic inflammation and impact ICB efficacy.
  • To elucidate the mechanisms by which macrophages mediate inflammation-induced ICB resistance in UC.

Main Methods:

  • Analysis of plasma IL-6 and CRP levels in relation to tumor macrophage infiltration across multiple ICB-treated UC cohorts.
  • Single-cell and bulk RNA sequencing of the largest UC patient atlas to date to characterize TME composition.
  • Spatial and functional analyses to assess the activity and interactions of identified macrophage subsets.

Main Results:

  • Elevated plasma IL-6 and CRP levels were associated with increased tumor macrophage infiltration in UC.
  • A subset of immunosuppressive SPP1+ macrophages was enriched in TMEs of patients with high plasma IL-6.
  • SPP1+ macrophages were found to suppress T cell activity via IL-6 signaling, while CXCL9+ macrophages promoted T cell activation.

Conclusions:

  • Systemic inflammation is linked to local immune dysfunction in the UC TME, characterized by an increase in immunosuppressive macrophages.
  • A macrophage-driven axis involving IL-6 signaling contributes to ICB resistance in urothelial bladder cancer.
  • Targeting SPP1+ macrophages presents a potential therapeutic strategy to enhance immunotherapy outcomes in UC.