In memoriam: Professor Brian Maurice John Foxwell, 1956 to 2008

Brian's research interests and accomplishments were wide ranging, and this enabled him to see links between different projects. He was not interested in the latest fashions, and he had strong views about the correct approaches to science. Two particular examples of approaches that he fought against was the use of transformed cell lines as models for use in cell signalling studies. He argued that with abnormal chromosome composition and hence huge genetic differences from normal cells, and cells dividing much faster than normal, how could their signalling pathways be representative? His major research contributions have resulted in the development of pioneering new approaches, for example using adenoviral vectors to induce transgene expression in primary cells that have traditionally been difficult to transfect. This technology was used to elucidate signal transduction mechanisms in primary cells and RA disease tissue. Professor Foxwell showed that there was heterogeneity in the signals that regulate tumour necrosis factor expression in human macrophages and those in diseased RA tissue, some being highly dependent on nuclear factor-κB and others much less so. This technology was used widely in his research activities and included identifying the target of action of STAT3 (signal transducer and activator of transcription 3) in interleukin-10 signalling using adenovirus-based tumour necrosis factor promoter constructs, as well as defining a new approach to vaccines by incorporating signals that activate the immune system (adjuvants) and the epitopes into one construct.More recently, Professor Foxwell developed an interest in what was then an emerging family of innate immune receptors, the Toll-like receptors (TLRs). He considered the possible involvement of these receptors in the pathology of RA, and studies using the adenoviral technology in RA diseased tissue provided strong evidence that TLRs do play a role in RA, and that these receptors could prove to be therapeut