MiStImm

MiStImm simulates self–nonself discrimination and humoral adaptive immune dynamics using an agent-based, stochastic model.

Key Features:

• Agent-Based Framework: MiStImm implements an agent-based model of the humoral adaptive immune response.
• Modeled Components: It explicitly represents T cells, B cells, antibodies, danger signals, interleukins, self cells, and foreign antigens.
• Temporal Simulation: Simulations progress in discrete time steps driven by stochastic events beginning post-conception.
• Comparative Models: MiStImm implements and compares a Conventional Immune Model and a One‑Signal T‑Cell Model.
• One‑Signal T‑Cell Hypothesis: The One‑Signal model encodes low-affinity complementary interactions between T-cell receptors (TCRs) and major histocompatibility complex (MHC) molecules on host cells.
• Visualization and Analysis Tools: It includes integrated tools for visualization and analysis of simulation outcomes.

Scientific Applications:

• Model Comparison: Model and compare alternative immune-response paradigms, including Conventional and One‑Signal models.
• Self–Nonself Discrimination: Investigate mechanisms of self–nonself discrimination in adaptive immunity.
• TCR–MHC Interaction Studies: Explore the role of low-affinity TCR–MHC complementary interactions and their contribution to a dynamic steady state.
• Immune Memory and Autoimmunity: Examine development of immune memory and conditions that avoid autoimmune reactions within simulated models.
• Pathogen Defense Mechanisms: Study how a limited genomic repertoire can defend against mutating pathogenic DNA via modeled immune dynamics.
• Clinical Comparison: Compare simulation outcomes with clinical observations in immunotherapy to generate mechanistic hypotheses.

Methodology:

Agent-based stochastic simulation advancing in discrete time steps, explicitly modeling T cells, B cells, antibodies, danger signals, interleukins, self and foreign cells, and implementing both Conventional and One‑Signal T‑Cell models including low‑affinity TCR–MHC interactions.