A model of auto immune response.

BACKGROUND: In this work, we develop a theoretical model of an auto immune response. This is based on modifications of standard second messenger trigger models using both signalling pathways and diffusion and a macro level dynamic systems approximation to the response of a triggering agent such as a virus, bacteria or environmental toxin.

RESULTS: We show that there, in general, will be self damage effects whenever the triggering agent's effect on the host can be separated into two distinct classes of cell populations. In each population, the trigger acts differently and this behavior is mediated by the nonlinear interactions between two signalling agents.

CONCLUSION: If these interactions satisfy certain critical assumptions this will lead to collateral damage. If the initial triggering agent's action involves any critical host cell population whose loss can lead to serious host health issues, then there is a much increased probability of host death. Our model also shows that if the nonlinear interaction assumptions are satisfied, there is a reasonable expectation of oscillatory behavior in host health; i.e. periods of remission.