Tregs suppress effector T cells largely without touching them directly. They constitutively express very high levels of the high-affinity IL-2 receptor α-chain CD25, so they out-compete effector T cells for the shared cytokine IL-2, which effector cells need to keep signalling through STAT5 and survive. This is the "cytokine-deprivation" model of Treg suppression (Pandiyan et al., 2007).
IL-2 concentration C(x,t) in the tissue obeys a reaction-diffusion equation, solved here on a 3D voxel grid each frame:
∂C/∂t = D·∇²C + S·[activated Teff] − Vmax·C/(C+Km)
The consumption term Vmax·C/(C+Km) is Michaelis–Menten receptor-mediated uptake — the same saturating kinetics as real CD25 binding — with Vmax set by local Treg + Teff density and the avidity slider (Tregs consume several-fold faster per cell).
Each effector cell accumulates a survival "signal" when local C is above a STAT5-signalling threshold, and loses it below threshold; when the signal hits zero the cell undergoes cytokine-withdrawal apoptosis (Bim-mediated) and fades out. New naive effector cells trickle in slowly, so the surviving population settles into an equilibrium set by the balance of secretion, diffusion and Treg consumption — raise Treg count or avidity and watch the steady-state effector population, and free IL-2, collapse.
- Treg count — number of high-affinity IL-2 sinks in the tissue.
- CD25 avidity — how fast each Treg consumes local IL-2 relative to an effector cell.
- Antigen stimulation — how much IL-2 activated effector cells secrete (a stronger immune trigger).
- Tissue diffusion — how quickly IL-2 spreads away from its source instead of staying locally concentrated.
Real-world relevance: this exact IL-2-sink mechanism is why low-dose IL-2 therapy (which favors Tregs, their receptor is far more sensitive) is used to calm autoimmune disease, while high-dose IL-2 (which reaches lower-affinity receptors on effector/NK cells too) is used to boost anti-tumor immunity.