• posterior uveitis
• birdshot retinochoroidopathy

Continuing our understanding of the basic pathobiology of non-infectious posterior segment intraocular inflammatory conditions has relied largely on experimental models of uveitis, such as experimental autoimmune uveoretininitis (EAU). Arguably such models are not well supported by human data in that there is still no definitive evidence of a role for retinal autoantigens in posterior uveitic conditions,^1,2 despite us moving on to clinical trials of tolerance induction.³ On the other hand the models are useful. The pathological changes observed appear to explain what we may see clinically—namely, vitritis, retinal vasculitis, chorioretinal leucocytic infiltrates, and optic nerve head and macula oedema.^4,5 As such we are able to discern common immune mediated processes that lead to inflammation, in particular T cell and macrophage behaviour, cytokine mediation of inflammatory response, and other immune regulatory mechanisms in play in the eye.⁶ To this end, preclinical studies of novel immune modulatory agents (a classic example being cyclosporin⁷) have now been successfully translated into clinical practice.⁸ There are caveats in our interpretations. Although in animal models the photoreceptors are the target tissue for retinal antigen specific autoreactive T cells …