Each T-cell that touches a cancer cell rolls an engagement probability. Cancer cells display PD-L1, which binds the T-cell's PD-1 receptor and suppresses the attack (immune checkpoint) — this is the same brake tumours exploit in real biology.
P(kill) = P_base(affinity) × (1 − PD-L1 × (1 − blockade))
- Checkpoint blockade — simulates anti-PD-1/PD-L1 drugs (e.g. pembrolizumab) that block the PD-L1 brake, restoring T-cell killing.
- CAR-T boost — engineered receptors raise base affinity so T-cells recognise and engage tumour antigen far more reliably, checkpoint or not.
- T-cell count — size of the immune force patrolling the tumour (a stand-in for lymphocyte infiltration).
- PD-L1 expression — how strongly the tumour displays its "don't kill me" signal.
- Tumour growth rate — how fast new cancer cells divide, competing against the kill rate.
Real-world relevance: checkpoint inhibitors and CAR-T therapy have transformed outcomes in melanoma, lung cancer and some leukaemias by re-arming the immune system against tumours that had learned to hide from it.