ABSTRACT
The retina is considered a site of immune privilege, where immune responses must be controlled to protect vision. To achieve this, the need for immune surveillance to counteract infection must be balanced against the need to control potentially sight-damaging inflammation. A physiochemical barrier that restricts normal leukocyte diapedesis is provided by the blood –retina barrier, and soluble factors and immunomodulatory ligands on ocular-resident cells, designed to regulate immune responses locally and systemically, are well described and reviewed (1). More recently, it has become clear that ocular resident cells with antigen-presenting ability are programmed to suppress or tolerise infiltrating
T cells rather than activate them (2-5). Despite these multiple mechanisms, ocular inflammation involving the retina and uveal tract is not uncommon (5,6), indicating that the dynamic interactions between the cells and tissues of the eye and the immune system maintaining privilege can break down in response to infection or immune dysfunction. Posterior uveitis, the mononuclear cell inflammation of the retina and uveal tract that can result, is thought to represent an autoimmune response to retinal antigens (5,7,8), and in this review we examine some data supporting the notion that endogenous posterior uveitis (EPU) represents an autoimmune response. In addition, we will briefly consider the evidence for local priming of T cells to retinal autoantigens and evidence for local regulation of the response.
