Complete Mechanics of Type 1 Diabetes Autoimmune Attack, a Mathematical Stopping Criterion, and Five Strategies Achieving Immune Quiescence

We present CIG-v5, a 10-variable ordinary differential equation (ODE) model capturing the complete mechanism of the Type 1 Diabetes (T1D) autoimmune attack across three anatomical compartments (pancreatic lymph node, islet tissue, peripheral blood) and four immune populations (stem-like memory T cells, effector T cells, regulatory T cells, and the inflammatory milieu). The model identifies three mutually reinforcing positive feedback loops — antigen-driven priming (L1), costimulation-dependent expansion (L2, dominant), and Treg depletion (L3) — whose interaction sustains the attack indefinitely. The system exhibits bistability between a tolerant and an autoimmune fixed point. Systematic parameter-space scanning reveals three dynamical regimes: A (active attack), Bm (managed), and Bq (quiescent/immune silence). We derive a mathematical stopping criterion: costimulation must be blocked ≥95% AND beta cells modestly protected, maintained indefinitely. This achieves 100% Bq in 300/300 Monte Carlo runs (±15% parametric perturbation). Five novel therapeutic strategies achieve Bq, including H9 (Inflammation Quench: infliximab + tocilizumab + anakinra) using exclusively approved drugs. The model was calibrated on 679 patients (R²=0.988) and validated on independent cohorts. All code is provided for full reproducibility. This deposit contains: the publication-ready paper (PDF), proof-of-concept Python code (CIG_v5_model.py), simulation results (JSON), and 5 publication-quality figures.