The transcription factor Nuclear Factor-kappa B is a biological component that is central to the regulation of genes involved in the innate immune system. Dysregulation of the pathway is known to be involved in a large number of inflammatory diseases. Although considerable research has been performed since its discovery in 1986, we are still not in a position to control the signalling pathway, and thus limit the effects of Nuclear Factor-kappa B within promotion of inflammatory diseases. We have developed an agent-based model of the Interleukin-1 stimulated Nuclear Factor-kappa B signalling pathway, which has been calibrated to wet-lab data at the single-cell level. Through rigorous software engineering, we believe our model provides an abstracted view of the underlying real-world system, and can be used in a predictive capacity through in silico experimentation. In this study, we have focused on the dynamics of the IKK complex and its activation of Nuclear Factor-kappa B. Our agent-based model suggests that the pathway is sensitive to: variations in the binding probability of the IKK enzyme to the inhibited Nuclear Factor-kappa B complex; and variations in the temporal rebinding delay of the IKK enzyme.
