Immune-mediated inflammation in the retina is regulated by a combination of anatomical, physiological and immuno-regulatory
mechanisms, referred to as the blood–retina barrier (BRB). The BRB is thought to be part of the specialised ocular microenvironment
that confers protection or “immune privilege” by deviating or suppressing destructive inflammation. The barrier between the
blood circulation and the retina is maintained at two separate anatomical sites. These are the endothelial cells of the inner
retinal vasculature and the retinal pigment epithelial cells on Bruch’s membrane between the fenestrated choroidal vessels
and the outer retina. The structure and regulation of the tight junctions forming the physical barrier are described. For
leukocyte migration across the BRB to occur, changes are needed in both the leukocytes themselves and the cells forming the
barrier. We review how the blood–retina barrier is compromised in various inflammatory diseases and discuss the mechanisms
controlling leukocyte subset migration into the retina in uveoretinitis in more detail. In particular, we examine the relative
roles of selectins and integrins in leukocyte interactions with the vascular endothelium and the pivotal role of chemokines
in selective recruitment of leukocyte subsets, triggering adhesion, diapedesis and migration of inflammatory cells into the
retinal tissue.
Keywords Blood–retina barrier - Retinal pigment epithelium - Selectins - Integrins - Chemokines - Tight junctions - Leukocytes - Lymphocytes - Monocytes - Inflammation - Uveitis