Immunotherapy Simulator | mysimulator.uk

Tumor Immune Response

Checkpoint inhibitor strength 0.40

T-cell count 18

Tumor growth rate 0.40

Cancer cells destroyed

Active cancer cells

–

T-cell activation

–

Avg shield level

–

How it works

Cancer cells display PD-L1 on their surface, which binds the PD-1 receptor on nearby T-cells and switches off the attack signal — the translucent yellow shell around each red cell is that checkpoint shield. A T-cell that gets close enough keeps "pressing" against the shield every frame; a checkpoint inhibitor drug blocks the PD-L1/PD-1 handshake, so the stronger the inhibitor, the faster the shield erodes and the sooner the cell is destroyed. Untreated (inhibitor near 0), most cells regenerate their shield faster than a lone T-cell can wear it down.

Δshield = -dt · engaged · (0.05 + inhibitor · 0.55)
kill when shield ≤ 0
activation % = engaged T-cells / active T-cells

Checkpoint inhibitor strength — how completely the drug blocks PD-L1/PD-1 suppression; higher values let T-cells tear through the shield instead of being switched off.
T-cell count — the size of the recruited immune force patrolling the tumor; more cells find and engage cancer cells faster.
Tumor growth rate — how quickly new cancer cells appear; a fast-growing tumor can outpace a weak or unaided immune response.
PD-L1 shields toggle — hide the shield shells to see the bare cancer cells and T-cell contacts more clearly.

Real-world relevance: this loop mirrors why checkpoint inhibitors (e.g. anti-PD-1/PD-L1 antibodies) can turn an immune system that already recognizes a tumor — but is being held back — into one that clears it, and why tumors that grow faster than the immune response can still escape.

T-cell Cancer cell PD-L1 shield Engaged T-cell

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