- CTL
- Treg
- Dendritic cell
- MDSC
- Tumour Cell
- NK cell
- Fibroblast
- Pericyte
- Platelet
- Eosinophil
- Granuloczte
- Mast cell
- B cell
- Macrophage
7+8 = Mesenchy malorigin
The tumour microenvironment (TME) consists of different cellular, including immune cells, and non-cellular components in and around the tumour. The TME has been recognised to play a significant role in tumour progression.1,2
The TME shapes tumour evolution (whether the tumour regresses, develops resistance, evades the immune system and/or metastasizes) and consequently impacts patient outcomes.3 An association has been observed between the levels of tumour infiltrating immune cells, key components of the TME, and patient prognosis: a colorectal cancer study showed that higher levels of tumour infiltrating CD3+ immune cells were associated with better disease free survival.4
Aberrant expression of PD-L1 on tumour cells has been reported to impede anti-tumour immunity, resulting in immune evasion.5 Therefore, interruption of the PD-L1/PD-1 pathway represents an attractive strategy to reinvigorate tumour-specific T cell immunity suppressed by the expression of PD-L1 in the TME. This approach has proven effective: PD-L1 expression on immune cells in the TME has been shown to identify urothelial cancer patients who are most likely to benefit from atezolizumab an anti-PD-L1 drug.6
References