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About the unit
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Inflammatory eye disease group
Inflammatory Eye Disease caused by immune attack on the retina, is a major cause of severe visual impairment. In some studies it has been estimated to account for 10-15% of all cases of total blindness, despite the low incidence of disease. The group's current projects are led by Professor Andrew Dick and Dr Lindsay Nicholson and include regulation of macrophage activity systemically and in the eye, particularly looking at cognate regulation of macrophage activity. Continued work on the central role of retinal microglia in immune regulation of retinal inflammation and repair is expanding with further reference to role of microglia, retinal macrophages and choroidal dendritic cells during experimental models of gene therapy in murine models of degeneration (in collaboration with Dr Robin Ali, institute of Ophthalmology, University of London).
Severe non-infectious posterior intraocular inflammation resulting in profound loss of vision.
Clinical translatory programmes have included in the past a randomised control trial of tacrolimus versus cyclosporin therapy for non-infectious posterior intraocular inflammation (uveitis) and phase I/II study of sTNFr therapy in severe refractory uveitis in collaboration with Therapeutic Antibody Centre, University of Oxford. Currently we are undertaking a randomised control trial of optimising Tacrolimus therapy and investigating steroid resistance (Professor Dick and Dr Lee). On-going work also with Molecular Ophthalmology unit (Dr Amanda Churchill and Dr Denize Atan) continues with investigation of the influence of genetic polymorphisms on severity and prognosis of uveitis.
More recently we have developed from Human donor eyes the ability to harvest retinal neural progenitor cells (NPC) capable of differentiating into retinal elements in vitro. This group (Dr T Qiu and Dr D Carter) in addition to studying the biology of NPC and the potential for retinal remodelling and regeneration, are looking at the ways NPC activity and differentiation is modulated by the retinal environment, particularly microglia during inflammatory responses.
Experimental model of Non-infectious posterior segment intraocular inflammation (Experimental autoimmune uveoretinitis), that parallels the destruction of the retina and the choroidal inflammation observed in man.
- Link to the Nicholson Group web site
- Work is supported by Iris Fund, National Eye Research Centre, Guide Dogs for the Blind Association, University of Bristol PhD scholarship and Fujisawa ltd.