The simulator demonstrates how regulatory T cells use three concurrent mechanisms, IL-2 competition, CTLA-4-mediated costimulation blockade, and IL-10/TGF-beta secretion, to suppress effector T cell activation, and shows how shifting Treg number or activity along a spectrum moves the system between autoimmune-prone and immunosuppressed states.
Adjust the sliders controlling Treg population density, CTLA-4 expression level, ambient IL-2 concentration, and secreted IL-10/TGF-beta output, then observe how effector T cell activation and proliferation respond in the simulation window. Try pushing Treg activity to its minimum to trigger runaway effector expansion resembling autoimmunity, then to its maximum to observe effector suppression resembling tumor immune evasion, to explore the full balance the system represents.
Sliders for Treg population density, CTLA-4 expression level, ambient IL-2 concentration, and IL-10/TGF-beta secretion rate, plus a readout of resulting effector T cell activation and proliferation.
Low-dose IL-2 therapy is used clinically to selectively expand a patient's own Tregs for treating autoimmune disease, while high-dose IL-2 does the opposite by also boosting effector and natural killer cells, showing how the same molecule can push the balance in either direction depending on dose.
The simulator demonstrates how regulatory T cells use three concurrent mechanisms, IL-2 competition, CTLA-4-mediated costimulation blockade, and IL-10/TGF-beta secretion, to suppress effector T cell activation, and shows how shifting Treg number or activity along a spectrum moves the system between autoimmune-prone and immunosuppressed states.
The simulator demonstrates how regulatory T cells use three concurrent mechanisms, IL-2 competition, CTLA-4-mediated costimulation blockade, and IL-10/TGF-beta secretion, to suppress effector T cell activation, and shows how shifting Treg number or activity along a spectrum moves the system between autoimmune-prone and immunosuppressed states.
Adjust the sliders controlling Treg population density, CTLA-4 expression level, ambient IL-2 concentration, and secreted IL-10/TGF-beta output, then observe how effector T cell activation and proliferation respond in the simulation window. Try pushing Treg activity to its minimum to trigger runaway effector expansion resembling autoimmunity, then to its maximum to observe effector suppression resembling tumor immune evasion, to explore the full balance the system represents.
Low-dose IL-2 therapy is used clinically to selectively expand a patient's own Tregs for treating autoimmune disease, while high-dose IL-2 does the opposite by also boosting effector and natural killer cells, showing how the same molecule can push the balance in either direction depending on dose.