Investigators and Projects
The desire to further my understanding of how the retina is damaged following injury, inflammation or degeneration comes from the relative inadequacies and frustrations of current treatments for patients with blinding diseases. This drive originated from the time I was a physician in training and looking after patients with inflammatory multisystem disease; although treatment was often beneficial for other organs, when the eye was affected, poor vision often developed. Since specialising in ophthalmology, my training has allowed me to develop my clinical expertise in caring for patients with inflammatory eye disease, whilst using my scientific training to generate and develop better treatments.
Although inflammatory eye disease is relatively rare compared to diabetic eye disease, it remains a leading cause of blindness and affects mainly working age people. The main causes in developed countries are autoimmune in origin and immunosuppression is frequently used to prevent blindness. Furthermore, it was apparent to me early in my studies of inflammatory eye disease, that despite differences in aetiology, T cell mediated autoimmune injury, retinal degeneration, age related degeneration or injury, and retinal destruction, follow a common pathway where macrophage activation was central.
I undertook my research and clinical training with the pre-eminent clinical ophthalmologist and ocular immunologist, Professor John Forrester in Aberdeen, and then went as a post-doc to work with Dr Jon Sedgwick at the Centenary Institute of Cancer Medicine and Cell Biology in Sydney Australia. My work in both Scotland and Australia led to long standing collaborations which continue today.
I developed methods of isolating and understanding the mechanisms of resident macrophage (microglia) and infiltrating macrophage activation in the retina (Brit J Ophthalmol 79; 834-840, Invest Ophthalmol Vis Sci 43 (7): 2250-2257). At the same time I was keen to develop approaches to suppress macrophage activation which has resulted in the development of anti-TNF therapies for ocular inflammation (Eur J Immunol . 26; 1018-1025., Arch Ophthalmol 122: 845-51).
Since my arrival in Bristol in 2000, I have continued to develop this interest, which is now considerably strengthened by the partnership with Lindsay Nicholson investigating the control (cytokine, cognate and matrix) of macrophage activation, macrophage interaction with T cells and the development of potential therapies to suppress macrophage activation and tissue damage (J Leuk Biol 74: 161-6. Amer J Path. 161(5):1669-77).