The NF-kappaB stress signalling system has an important role in the control of inflammation, being both stimulated by cytokines and itself regulating cytokine gene expression. NF-kappaB dynamics have previously been studied in a variety of different cell lines and primary cells. It has been shown, using live-cell microscopy, that NF-kappaB proteins show complex oscillatory dynamics between the nucleus and cytoplasm at the single-cell level. These dynamics are thought to control gene expression responses. A key aim of the work described in this thesis was to understand the functional NF-kappaB-mediated paracrine interactions that occur between different cell types to control tissue-level inflammatory responses. This project aimed to investigate cytokine-mediated interactions between neural progenitor cells (NPCs) and microglia following Tumour Necrosis Factor alpha (TNFalpha) stimulation. Specifically, the interactions between the C17.2 NPC line and the BV.2 microglial cell line were used as a model system. Understanding the interactions between these cell types might be physiologically important for providing an insight into the regulation of neuroinflammation. A further goal was to establish a better understanding of how single-cell NF-kappaB dynamics could be related to differential gene expression and cell survival. Initially, different methods for expressing labelled RelA/p65 (p65) in C17.2 and BV.2 cells were investigated. TNFalpha-induced NF-kappaB activation and p65 dynamics were measured in cells that had been transfected or transduced with a range of p65 constructs (plasmid, bacterial artificial chromosome or lentiviral vectors) to express fluorescent p65 fusion proteins. This study resulted in the selection of lentivirally transduced cells, expressing p65-eGFP, as the most appropriate model system for the observation of p65 dynamics in these cells. C17.2 and BV.2 p65 dynamics and C17.2 NF-kappaB transcriptional activity were measured in mono-cultures and co-cultures. These data indicated that BV.2 cells mediated inhibition of TNFalpha-induced NF-kappaB activity and p65 nuclear translocations in the C17.2 NPCs. Preliminary evidence for C17.2 regulation of BV.2 p65 dynamics was also found. However, this project mainly focussed on modulation of the C17.2 cell responses, since it was considered that these were likely to be particularly important in the control of neuroinflammation.Gene expression was measured in untreated and TNFalpha-stimulated mono-cultures, co-cultures and transwell co-cultures, in order to assess the functional effects of any intercellular interactions. These studies were also designed to assess the outcome of TNFalpha treatment and co-culture interactions on cell viability and apoptosis. In addition to this, an NF-kappaB inhibitor was used to evaluate the NF-kappaB contribution to changes in cell viability and apoptosis. These results implicated a role for TNFalpha in C17.2 apoptosis and suggested that the presence of BV.2 cells could prevent this cell fate. Interestingly, NF-kappaB inhibition was also shown to induce C17.2 apoptosis and increased overall viability. This may suggest promotion of cell proliferation. Together, these data provide functional evidence for TNFalpha-induced, co-culture- and NF-kappaB-mediated interactions between these cell types at the molecular, genetic and cellular level. These interactions had a significant effect on the extent of cell survival in response to TNFalpha. This observation is relevant to the study of neurodegenerative disease, where high TNFalpha concentrations are known to mediate tissue damage and NPCs have been shown to provide a therapeutic benefit.