Thygesons Superficial Punctate Keratopathy

HLD DR3 antigen affects response to Thygeson’s Superficial Punctate Keratitis

In 1981, Richard W. Darrell, MD, reviewed literature relating to TSPK and its association with a histocompatibility antigen HLA DR3.  Both HLA D and HLA DR antigens are associated with the immune response genes, and HLD DR3 antigen may interfere with the immune response of patients of Thygeson’s Superficial Punctate Keratitis to endogenous and exogenous viral infections, which results in the prolonged course and remission and exacerbations that have become characteristic of the disease.

Research with inbred strains of mince shown that the immune response genes are located within the major histocompatibility complex, the H2 system, known as the HLA in humans with the immune response genes mapping within the HLA D and HLA DR regions.

Cellular and serologic methods were used to define the various molecules and antigens encoded by HLA genes.  The HLA A, HLA B, and HLA C antigen loci code are present on the surface of all nucleated cells of the body as well as on platelets.  Typing for antigens that are coded by these three loci was carried out by complement mediated microcytotoxicity assay (which was done by incubating the lymphocytes from the person being tested with known antisera), and then the cells are tested by a dye exclusion technique to look for positive reactions, or cytolysis, indicating the phenotype of HLA A, HLA B, and HLA C of the cells.

However, HLA D antigens are limited in their distribution, as they are found on B nor on resting T lymphocytes, and they were found using cellular rather than serologic techniques.  The person to be tested has their lymphocytes grown in a culture with homozygous typing cells (HTC) of all known varieties of HLA D, and then the phenotype is given based on negative reactions to specific HTCs.

A number of diseases are associated with increased frequency of HLA Dw3 and HLA DR3 antigents including gluten-sensitive enteropathy, chronic hepatitis, dermatitis herpetiformis, Addison’s disease, insulin-dependent diabetes mellitus, Graves’ disease, Sjogren’s syndrome, and systemic lupus erythematosis. The relative risk for a person carrying HLA DR3 of developing some of these diseases compared with controls, provides a risk of 2.2 for chronic active hepatitis, 2.7 for myasthenia gravis, 3.3 for insulin-dependent diabetes mellitus, and17.5 for coeliac disease, and 5.65 of developing TSPK

Thygeson’s Superficial Punctate Keratitis may be caused by a virus whose clinical effect on the epithelium of the cornea and stroma is found by the presence of HLA DR3.  Immune responses are found by the presence of lymphocytes in corneal lesions, which are found by electron microscopy, by the marked effects of corticosteroids and by the chronic nature of TSPK with exacerbations and remissions.

The research concluded that the frequency of histocompatability antigen HLA DR3 is significantly increased in patients with Thygeson’s Superficial Punctate Keratitis (the relative risk = 5.6 p<0.001).  As the antigen is associated with several autoimmune diseases, then it makes sense to suggest that the immune mechanisms also play a significant role in Thygeson’s Superficial Punctate Keratitis.

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