Alemtuzumab and T-cell network recovery

Group 1 — common colored continuous configuration

Declared continuous network context with formal model marking units and explicit pretreatment history.

Readouts

TH1 · dimensionless

TH1 over the selected simulation window.

TH17 · dimensionless

TH17 over the selected simulation window.

Regulatory T-cell · dimensionless

Regulatory T-cell over the selected simulation window.

Cns effector regulatory proxy · dimensionless

Cns effector regulatory proxy over the selected simulation window.

Study purpose

• How do the model's key biological readouts change under group 1 — common colored continuous configuration?

Assumptions

• Continuous reconstruction with ordinary mass action x^m/m! and directly transcribed custom reaction rates; no stochastic distribution or fitted-patient replay.
• State values are formal dimensionless model markings. Treatment is an abstract scaled marking, not mg, mol, concentration or receptor occupancy.
• The colored configuration has self-Th17 passage kBBB*Th17^2/2 with net loss of one Th17 and entry of one CNS effector. Separate constitutive configurations add one to each pool at rate kBBB.
• Both regulatory duplication transitions use peripheral Th1. Effector-antigen killing consumes both antigen and the effector; regulatory and treatment killing return their catalysts.
• Raw day0 starts180days before treatment; full horizon2520days corresponds to clinical day−180..2340, including six months beyond the observed72month follow-up.
• Two course-level marking jumps occur at raw days180/540. An additional what-if course occurs at1260; within-course daily administrations and infusion pharmacokinetics are not modeled.
• The alternate forcing has a Gaussian input-rate envelope centered at raw1230days, width147days. Neither this center nor the integrated antigen maximum is asserted to match a clinical month30 peak.
• CNS pools have no exit in the specified network. Their regularized ratio is an exploratory network proxy, not measured CNS damage or relapse probability.
• The normalized immune denominator is positive in admitted contexts; a numerical zero extension does not define a new empty-system biological model.
• No individual random effects, original clustering, calibration uncertainty, statistical likelihood or clinical optimization is reproduced.