The uveal tract represents the vascular organ of the eye, providing a conduit for inflammatory cells to enter the eye. The ocular compartments, including the uveal tract, are relatively immune-privileged sites. As such, they are characterized by anatomical, cellular, and molecular factors that protect the eye from inflammation-induced visual loss. Similar to the brain, the eye has a blood-tissue barrier consisting of tight junctions between endothelial cells, as well as the ocular pigment epithelial layers. Although these barriers reduce the likelihood of a pathogen gaining entrance to the eye, they are not absolute, and viruses, bacteria, and parasites have evolved distinctive mechanisms to exploit these specialized properties. The eye has developed several strategies to modify the innate and adaptive immune system to create immune privilege: immunological ignorance, anterior-chamber-associated immune deviation (ACAID), and an intraocular immunosuppressive environment. In the eye, the absence of lymphatic drainage pathways is a means by which ocular antigens are shielded from the immune system. In addition, corneal cells lack MHC class II expression and show reduced class I major histocompatibility complex (MHC) expression, thwarting the ordinary process of antigen presentation and activation of CD4+ and CD8+ T-cells (5).
Antigens gaining access to the anterior chamber elicit a deviant systemic immune response termed ACAID. This response can prime CD8+ T-cells and generate noncomplement-fixing antibodies, but a more robust stimulus is avoided through mechanisms that interfere with the activation of CD4+ T helper 1 (TH1) and T helper 2 (TH2) cells, and activation of B-cells secreting complement-fixing antibodies. ACAID also is a feature of the immune response in the vitreous cavity and subretinal space.
The eye also produces both soluble and cell-surface factors that suppress the immune response. These soluble factors convey various anti-inflammatory and immuno-suppressive properties and include transforming growth factor-p2 (TGF-p2), a-melanocyte-stimulating hormone, vasoactive intestinal peptide, calcitonin gene-related peptide, thrombospondin, macrophage inhibitory factor, interleukin-1 (IL-1) receptor antagonist, inhibitors of complement activation, and CD95 ligand. Ocular cells also express molecules on their surface that promote apoptosis of CD95+ T-cells, inhibit complement activation, and inhibit T-cell activation (5,6).
Despite its immune-privileged status, uveal inflammation may be stimulated by environmental antigens or autoantigens. Environmental triggers can be biological, physical, or chemical. Physical trauma in one eye may lead to delayed ocular inflammation in both the injured and contralateral eye; the inflammation in the noninjured eye is called "sympathetic ophthalmia." The occurrence of this syndrome has led to the concept that eye-restricted autoantigens can provoke an inflammatory response. In animal models, uveitis can be elicited by several means: injection of nonocular-derived antigens, injection of retinal autoantigens (e.g., experimental autoimmune uveoretinitis), and injection of ocular but nonretinal autoantigens. There is evidence for autoimmunity in humans with uveitis, but so far no causal link has been established between retinal autoantigens as triggers and the pathogenesis of uveitic conditions. In several studies, patients with uveitis have shown cellular responses to retinal antigens. Sera from patients with uveitis may also contain autoantibodies to retinal proteins (e.g., antiretinal antibodies) (6).
HLA associations have been found with certain types of uveitis. For example, HLA-B27 has been associated with acute anterior uveitis and HLA-A29 with Birdshot retinochoroidopathy. HLA-B27 is expressed by 70% to 90% of patients with acute anterior uveitis and spondyloarthropathy, and by about 50% of patients with acute recurrent anterior uveitis lacking features of a spondyloarthropathy. HLA-A29 is present in 80% to 98% of patients with Birdshot retinochoroidopathy, compared to only 7% of controls (7,8).
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