What determines the site of inflammation in uveitis and chorioretinitis?

Uveitis is a relatively confusing term since it implies primary inflammation of the uveal tract. However, it has become clear during the last few decades of research into the causes of uveitis that the uveal tract acts primarily as the conduit for the inflammatory cells and the increased blood flow that accompany inflammation targeted to other sites in the eye such as the retina and sclera. Uveitis is, therefore, better referred to as intraocular inflammation (l01). A major problem in understanding the pathophy­ siology of 101 is that clinically there is a great variety of presentations of apparently different conditions. However, a significant unifying concept, at least from the viewpoint of pathogenetic mechanisms, is that many of the clinical manifestations of 101 can be mimicked with models of experimental autoimmune uveoretinitis (EAU) which utilise a single antigen.1 This is not to say that autoimmune mechanisms account for most causes of 101 since the opposite is probably true; rather, that the intraocular tissues, particularly the retina and choroid, can respond to challenge by foreign or autoantigen in only a limited set of ways and that it should not be surprising that there is considerable overlap in the clinical manifes­ tations of many of these conditions. These concepts have been discussed previously?.3 This paper aims to address a separate but related problem: if the eye and its component tissues can respond in only a limited set of clinical manifesta­ tions, why is there preferential localisation of inflammation and tissue damage to discrete sites in certain conditions?