Immune Phenotypes

Unlocking cancer immunity for more patients

Analysing patient biopsies collected from clinical trials across multiple tumour types has led to a deeper understanding of the mechanisms of immune response and escape. These studies have illustrated a range of immune involvement within the tumour microenvironment.1,2

The Roche research team has identified 3 primary immune phenotypes that describe the level of T-cell presence and activity within the tumour microenvironment, and can help determine disruptions or mechanisms of immune escape in cancer immunity.1-3

3 immune phenotypes characterise the pattern of immune activity1,2,4

immune phenotypes

*Accumulation of CD8+ T cells that do not penetrate the tumour (arrows).
Abundance of CD8+ T cells within the tumour (arrows).
  • Immune desert
  • Immune excluded
  • Inflamed
Immune desert

No existing cancer immunity: cancer immunity cycle cannot be initiated (disruptions in steps 1-3)1,2,5



  • Absence of CD8+ T cells in the tumour microenvironment
  • Lack of preexisting antitumour immunity

Immune escape mechanisms1-3

  • Poor tumour immunogenicity due to low mutational load or lack of antigen release
  • Tumour cells and immunosuppressive cells (regulatory T cells, myeloid-derived suppressor cells, etc), may inhibit dendritic cells from properly activating T cells
  • Suboptimal T-cell activation due to disrupted costimulatory interactions
Immune excluded

Cancer immunity halted: active T cells cannot reach tumour cells (disruptions in steps 4-5)1,2,5



  • Abundance of immune cells in the tumour stroma
  • Preexisting antitumour immunity rendered ineffective due to poor T-cell infiltration or retention

Immune escape mechanisms1,2

  • High expression of receptors responsible for vasculogenesis and angiogenesis, such as VEGF
  • Low levels of ligands for CXCR3, a chemokine receptor that plays a large role in T-cell trafficking

Cancer immunity held in check: active T cells in tumour microenvironment are not functioning properly (disruptions in steps 6-7)1-3



  • Abundance of tumour-infiltrating immune cells, including CD4+ and CD8+ T cells
  • Presence of proinflammatory and effector cytokines
  • Higher mutational load
  • Preexisting antitumour immunity is arrested

Immune escape mechanisms1,3

  • Major histocompatibility complex not functioning normally or absent from cancer cells
  • High expression of checkpoint markers, such as PD-L1
  • Presence of immunosuppressive cells such as regulatory T cells and myeloid-derived suppressor cells
  1. Chen DS, Mellman I. Elements of cancer immunity and the cancer-immune set point. Nature. 2017;541:321-330. PMID: 28102259
  2. Kim JM, Chen DS. Immune escape to PD-L1/PD-1 blockade: seven steps to success (or failure). Ann Oncol. 2016;27:1492-1504. PMID: 272071083
  3. Hegde PS, Karanikas V, Evers S. The where, the when, and the how of immune monitoring for cancer immunotherapies in the era of checkpoint inhibition. Clin Cancer Res. 2016;22:1865-1874. PMID: 27084740
  4. Gajewski TF. The next hurdle in cancer immunotherapy: overcoming the non–T-cell–inflamed tumor microenvironment. Semin Oncol. 2015;42:663-671. PMID: 26320069
  5. Bacac M, Fauti T, Sam J, et al. A novel carcinoembryonic antigen T-cell bispecific antibody (CEA TCB) for the treatment of solid tumors. Clin Cancer Res. 2016;22:3286-3297. PMID: 26861458

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