Uveitis denotes inflammation of the uveal tract of the eye and is generally categorised as either anterior (involving the iris/ciliary body) or posterior (involving the choroid as well as adjacent structures including pigment epithelium and retina).1Although uveitis is a known cause of blindness, until recently there were few data reflecting the prevalence and incidence of uveitis among the blind, mainly because of the lack of information concerning the incidence of sight threatening complications from uveitis. One recent study has shown that the incidence of visual impairment in uveitis is 35% and is mainly due to posterior uveitis, largely as a result of persistent cystoid macular oedema.2 Other studies have shown that there is a 25% loss of vision in 4% of patients with anterior uveitis, 43% with posterior uveitis, and 40% with panuveitis.3 Moreover, specific uveitic syndromes—for example, Behçet’s disease45 and serpiginous chorioretinopathy,6 have a renowned poor prognosis without therapy. Suttorp-Schulten and Rothova7 have highlighted the socioeconomic impact of blindness due to uveitis, especially as most cases of visual impairment occur in the working age group, and uveitis now ranks with diabetic retinopathy as one of the major causes of visual handicap in this age group. As many uveitic entities are curable, or at least controllable in the sense that ocular damage can be prevented or limited with early and adequate therapy, we discuss a structured and rational approach to immunosuppression with respect to the control of intraocular inflammation, which aims to maintain best possible visual function while minimising therapy induced side effects, in particular those which occur with prolonged steroid therapy.