Although it has been recognised for a long time that bacterial and viral infection can account for some cases of uveitis, it has also been recognised that the majority of cases fail to show any evidence of this. Furthermore, in many instances the eye disease may be associated with known autoimmune disease elsewhere in the body. There are several different ways in which the uvea might be expected to become the focus of an antigen-antibody reaction. A foreign agent such as a virus might reside in the uvea and cause an antibody response, which coincidentally involves uveal tissue, or, on the other hand, a foreign agent might react with a specific marker on the cell membrane to produce a new active antigen. It is now recognised that patients who inherit certain of the human leucocyte antigens (HLA) are more susceptible to particular types of uveitis, for example the uveitis seen in ankylosing spondylitis and Reiter's disease (HLA-B27). It has been suggested that HLA might act as the specific marker in these cases. A further way in which the uvea might become the centre of an immune response concerns the question of self-recognition. It now appears that there is a mechanism in the body that normally prevents antibodies in the serum from acting against our own tissues. This active suppression is maintained by a population of thymus-derived lymphocytes (T lymphocytes) known as T-suppressor cells. There is evidence to suggest that sympathetic ophthalmitis might arise from inhibition of the T-suppressor cells after uveal antigens have been introduced into the bloodstream. Patients with juvenile rheumatoid arthritis occasionally develop uveitis, whereas rheumatoid disease in adults is more commonly associated with the dry eye syndrome and episcleritis.
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