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The eye has all the mechanisms necessary for detection and processing (afferent immune reaction) as well as adequate initiation of an (efferent) immune response. Apart from the typical antigen-processing cells, locally present elements (e.g. glial cells and retinal pigment epithelium) can also be involved in the afferent reaction. For the efferent mechanisms a complex regulative system exists, which includes cellular and humoral responses and is essentially determined by surface molecules. In addition, the ocular environment is rich in immunosuppressive molecules that contribute to the regulation of immune cells. The adaptation of the anatomical and biochemical mechanisms for the creation of an immune-privileged microenvironment makes this sense organ unique. The purpose of this article is to highlight the specific features of the eye and to establish a reference to frequent ocular manifestations in rheumatic diseases.

Eye involvement is a frequent finding in patients with rheumatoid arthritis and may represent the leading clinical manifestation of disease. In this context, all components of the visual organ might be affected. The main spectrum of eye involvement comprises keratoconjunctivitis sicca, episcleritis and scleritis as well as ulcerative keratitis. As with the underlying disease, autoimmune reactions based on a patient's genetic predisposition are assumed to be of significance in disease pathogenesis. Emerging evidence also points to additional morphological and physiological ocular characteristics in the pathogenesis of the various ocular pathologies. This article gives an overview of clinical aspects, pathogenetic background as well as therapeutic options for ocular involvement in rheumatoid arthritis.

Corneal and conjunctival biopsies of 13 patients with rheumatoid arthritis and corneal ulceration (RA-keratomalacia) have been characterized by immunohistological and histochemical analysis. Biopsies from 13 patients with bacterial conjunctivitis, 7 patients with allergic conjunctivitis, 15 patients with senile cataract and 15 patients with keratokonus served as controls. The phenotypic composition of the conjunctival inflammatory infiltration of rheumatoid corneal ulceration was not significantly different from the other inflammatory eye diseases studied. However, conjunctival epithelial cells of all RA-patients showed strong de novo expression of HLA-DR- and DP-antigens. HLA-DQ-antigens were only weakly expressed in a minority of patients. In bacterial conjunctivitis a less intense HLA-class-II-expression was found to be restricted to HLA-DR-antigens. Furthermore, in RA patients stromal fibroblasts of the cornea expressed lysosomal elastase. Both observations could be explained by paracrine action of interleukins produced by infiltrating T-lymphocytes and macrophages. Thus, it might be tempting to speculate that immunologically induced, elastase mediated autodegradation of corneal stroma may be an important factor in the pathogenesis of rheumatoid corneal ulceration.